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1
Ratti, Emiliangelo, David J. Carpenter, Stefano Zamuner, Sofia Fernandes, Lisa Squassante, Heidi Danker-Hopfe, Graeme Archer, et al. "Efficacy of Vestipitant, A Neurokinin-1 Receptor Antagonist, in Primary Insomnia." Sleep 36, no. 12 (December 1, 2013): 1823–30. http://dx.doi.org/10.5665/sleep.3208.
Повний текст джерела
2
Palve, Suchitra, and Sachin Palve. "Comparative study of self-directed learning and traditional teaching method in understanding cardio- respiratory physiology among medical undergraduates." Biomedicine 42, no. 1 (March 5, 2022): 138–42. http://dx.doi.org/10.51248/.v42i1.662.
Повний текст джерелаАнотація:
Introduction and Aim: Active and learner centred learning methods specially, self-directed learning is considered to be an important method of blended learning approach of imparting knowledge among under graduate medical students in new curriculum through integrated approach. The aim of the study is to analyse the impact and benefits of self-directed learning sessions for understanding cardio- respiratory physiology among phase one MBBS students. Design and Methods: This cross-sectional study was conducted among 250 students of Phase I MBBS for CVS and RS modules. Two groups of students were made Group A (n=125) was administered with self- directed learning sessions, while group B (n=125) was administered with normal didactic lecture session for the same topics. Following each session an objective assessment was conducted for all the topics covered in SDL and lecture sessions and the results were assessed and compared. Results: The maximum marks secured in objective assessment by Group A students post self-directed learning sessions for both cardiovascular and respiratory physiology modules were 31.2% (39/125) and 32.8% (41/125); while moderate marks were secured by 47.2% (59/125) and 48% (60/125). For assessment conducted after lecture sessions for both cardiovascular and respiratory physiology module, maximum marks were obtained by 25.6% (32/125) and 24% (30/125); while moderate marks were obtained by 21.6% (27/125) and 23.5% (29/125) respectively. Significant difference was found in the p values of marks for both modules(n=0.009) (n=0.008). The internal assessment scores showed considerable difference in the maximum marks obtained by students attending SDL sessions (80-89%) as compared to didactic learning sessions (70–79%) with p value = 0.0190, 0.01179 and 0.0192, a0.01184, respectively for both modules. Conclusion: Self-directed learning method seems to be more effective way of delivering the concept as compared to traditional lecture sessions.
3
Zak, Margie B., Carl F. Dmuchowski, and Maureen A. Smythe. "Laboratory Abnormalities in Patients in the Medical Intensive Care Unit." Journal of Pharmacy Technology 12, no. 1 (January 1996): 12–15. http://dx.doi.org/10.1177/875512259601200105.
Повний текст джерелаАнотація:
Objective: The goals of this article are to (1) identify the incidence of reported laboratory abnormalities in patients in the medical intensive care unit (ICU); (2) characterize the relationship between reported laboratory abnormalities and Acute Physiology and Chronic Health Evaluation III (APACHE III) score, length of stay, and mortality; and (3) evaluate therapeutic replacement in patients with electrolyte abnormalities. Design: Retrospective chart review of all patients admitted to the medical ICU between April 1, 1993 and June 30, 1993. Setting: Large teaching institution. Participants: Patients admitted to the medical ICU (n = 116). Interventions: The following data were collected: age, sex, admitting diagnosis, serum electrolyte and laboratory parameters, APACHE HI score, length of ICU stay, and mortality. Results: Ten individual laboratory abnormalities were found in more than 30% of all patients in the medical ICU (range 32.8–59.5%). Abnormalities in four laboratory parameters were associated with undesirable patient outcomes. Patients with hypoalbuminemia had a significantly higher APACHE HI score (p < 0.05). Hypocalcemia, hypomagnesemia, and hypoalbuminemia all were associated with an increased length of stay in the ICU (p < 0.05). Overall mortality was significantly higher in patients with alkalosis (p = 0.002). Therapeutic replacement in those with low electrolyte concentrations often was delayed or missed. Fifteen to 75% of patients who had abnormally low serum electrolyte concentrations were not treated. Conclusions: A high incidence of laboratory abnormalities is reported in patients admitted to the medical ICU. Several of these abnormalities are associated with undesirable outcomes such as an increased length of ICU stay in patients with hypoalbuminemia, hypocalcemia, and hypomagnesemia and increased mortality in patients with alkalosis. Therapeutic replacement of electrolytes in patients with abnormalities often was delayed or missed.
4
Boden, A. G., M. C. Harris, and M. J. Parkes. "Apneic threshold for CO2 in the anesthetized rat: fundamental properties under steady-state conditions." Journal of Applied Physiology 85, no. 3 (September 1, 1998): 898–907. http://dx.doi.org/10.1152/jappl.1998.85.3.898.
Повний текст джерелаАнотація:
Experiments were performed to measure the apneic threshold for CO2 and its fundamental properties in anesthetized rats under steady-state conditions. Breathing was detected from diaphragmatic electromyogram activity. Mechanical hyperventilation resulted in apnea once arterial[Formula: see text]([Formula: see text]) had fallen far enough. Apnea was not a reflex response to lung inflation because it did not occur immediately, was not prevented by vagotomy, and was reversed by raising [Formula: see text]without changing mechanical hyperventilation. The apneic threshold was measured by hyperventilating rats mechanically with O2 until apnea had occurred and then raising [Formula: see text] at constant hyperventilation until breathing reappeared. The mean[Formula: see text] level of the apneic threshold in 42 rats was 32.8 ± 0.4 Torr. The level of the threshold did not depend on the volume at which the lungs were inflated. The level of the threshold, under steady-state conditions, was the same when approached from hypocapnia as from eupnea. The level of the threshold could be raised by 9 Torr by chronic elevation of the eupneic [Formula: see text] level by 18 Torr.
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O'Connor, Sinéad, Paul McLoughlin, Charles G. Gallagher, and Helen R. Harty. "Ventilatory response to incremental and constant-workload exercise in the presence of a thoracic restriction." Journal of Applied Physiology 89, no. 6 (December 1, 2000): 2179–86. http://dx.doi.org/10.1152/jappl.2000.89.6.2179.
Повний текст джерелаАнотація:
In the presence of an externally applied thoracic restriction, conflicting ventilatory responses to exercise have been reported, which could be accounted for by differences in exercise protocol. Seven male subjects performed two incremental and two constant-workload ergometer tests either unrestricted or in the presence of an inelastic corset. Ventilatory variables and arterial estimates of Pco 2 were obtained breath by breath. Subjects hyperventilated in the presence of restriction during the constant-workload test (38.4 ± 3.0 vs. 32.8 ± 3.0 l/min for the average of the last 3 min of exercise, P < 0.05), whereas, at an equivalent workload during the incremental test, ventilation was similar to unrestricted values (unrestricted = 26.3 ± 1.6 vs. restricted = 27.9 ± 2.3 l/min, P = 0.36). We used a first-order linear model to describe the effects of change in workload on minute ventilation (24). When the time constants and minute ventilation values measured during unrestricted and restricted constant-workload exercise were used to predict the ventilatory response to the respective incremental exercise tests, no significant difference was observed. This suggests that hyperventilation is not seen in the restricted incremental test because the temporal dynamics of the ventilatory response are altered.
6
Scheuer, D. A., and M. H. Perrone. "Angiotensin type 2 receptors mediate depressor phase of biphasic pressure response to angiotensin." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 5 (May 1, 1993): R917—R923. http://dx.doi.org/10.1152/ajpregu.1993.264.5.r917.
Повний текст джерелаАнотація:
Angiotensin (ANG) can produce a biphasic arterial pressure response, i.e., an increase followed by a decrease. Because ANG type 1 (AT1) receptors mediate the pressor response to ANG, we hypothesized that the opposing depressor action is mediated by the ANG type 2 (AT2) receptors. In thiobutabarbital (Inactin)-anesthetized rats bolus injections of angiotensin III (ANG III; 100, 300, and 1,000 ng/kg iv) produced peak increases in MAP at 20 s of 13.4 +/- 1.4, 20.1 +/- 2, and 27.5 +/- 2.8 mmHg and maximum decreases in pressure at 120 s of -6.3 +/- 1.5, -6.8 +/- 2.2, and -11.4 +/- 4.9 mmHg. During blockade of the AT1 receptors with DuP 753 (losartan, 10 mg/kg) the increases in MAP were eliminated (P < 0.01), whereas the depressor responses (-24.7 +/- 8, -32.8 +/- 9.3, and -42.0 +/- 10.0 mmHg) were significantly (P < 0.05) larger. In separate groups of rats, combined blockade of both AT1 and AT2 receptors eliminated all changes in MAP in response to ANG III, whereas blockade of AT2 receptors alone enhanced the pressor response to ANG III. During AT1 receptor blockade angiotensin II also caused consistent decreases in pressure, which were inhibited during combined blockade of AT1 and AT2 receptors. Therefore, we have demonstrated that the AT2 receptors mediate a depressor response to ANG.
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Riedel, Thomas, John F. Fraser, Kimble Dunster, John Fitzgibbon, and Andreas Schibler. "Effect of smoke inhalation on viscoelastic properties and ventilation distribution in sheep." Journal of Applied Physiology 101, no. 3 (September 2006): 763–70. http://dx.doi.org/10.1152/japplphysiol.01635.2005.
Повний текст джерелаАнотація:
Smoke inhalation injuries are the leading cause of mortality from burn injury. Airway obstruction due to mucus plugging and bronchoconstriction can cause severe ventilation inhomogeneity and worsen hypoxia. Studies describing changes of viscoelastic characteristics of the lung after smoke inhalation are missing. We present results of a new smoke inhalation device in sheep and describe pathophysiological changes after smoke exposure. Fifteen female Merino ewes were anesthetized and intubated. Baseline data using electrical impedance tomography and multiple-breath inert-gas washout were obtained by measuring ventilation distribution, functional residual capacity, lung clearance index, dynamic compliance, and stress index. Ten sheep were exposed to standardized cotton smoke insufflations and five sheep to sham smoke insufflations. Measured carboxyhemoglobin before inhalation was 3.87 ± 0.28% and 5 min after smoke was 61.5 ± 2.1%, range 50–69.4% ( P < 0.001). Two hours after smoke functional residual capacity decreased from 1,773 ± 226 to 1,006 ± 129 ml and lung clearance index increased from 10.4 ± 0.4 to 14.2 ± 0.9. Dynamic compliance decreased from 56.6 ± 5.5 to 32.8 ± 3.2 ml/cmH2O. Stress index increased from 0.994 ± 0.009 to 1.081 ± 0.011 ( P < 0.01) (all means ± SE, P < 0.05). Electrical impedance tomography showed a shift of ventilation from the dependent to the independent lung after smoke exposure. No significant change was seen in the sham group. Smoke inhalation caused immediate onset in pulmonary dysfunction and significant ventilation inhomogeneity. The smoke inhalation device as presented may be useful for interventional studies.
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Koike, A., D. Weiler-Ravell, D. K. McKenzie, S. Zanconato, and K. Wasserman. "Evidence that the metabolic acidosis threshold is the anaerobic threshold." Journal of Applied Physiology 68, no. 6 (June 1, 1990): 2521–26. http://dx.doi.org/10.1152/jappl.1990.68.6.2521.
Повний текст джерелаАнотація:
We evaluated maximal O2 uptake (VO2max), the metabolic acidosis threshold determined by the V-slope analysis [plot of CO2 output (VCO2) as a function of oxygen uptake (VO2)], the ratio of increase in VO2 to work rate increment (delta VO2/delta WR), the upper slope (S2) of the V-slope analysis, and the VO2 for work below and above the metabolic acidosis threshold to determine whether the changes in O2 transport caused by increased carboxyhemoglobin (HbCO) affected these parameters and variables. Ten normal subjects (aged 32.8 +/- 7.1 yr) performed symptom-limited incremental exercise tests in a ramp pattern on a cycle ergometer while breathing air and air with added carbon monoxide to cause HbCO to be approximately 11% and 20%. VO2max decreased by 11.6 and 19.3%, the metabolic acidosis threshold decreased by 11.9 and 19.6%, delta VO2/delta WR decreased by 8.9 and 14.0%, and S2 increased by 13.6 and 21.8% when HbCO was increased to 11 and 20%, respectively. Most importantly, VO2 was unchanged related to work rate below the metabolic acidosis threshold during the tests with increased HbCO but was reduced at the work rates above the metabolic acidosis threshold. These findings are consistent with the concept that the metabolic acidosis threshold is synonymous with an anaerobic threshold, i.e., the latter demarcating the VO2 above which the contracting muscles are not adequately supplied with O2 but below which they are.
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Carolan, B., and E. Cafarelli. "Adaptations in coactivation after isometric resistance training." Journal of Applied Physiology 73, no. 3 (September 1, 1992): 911–17. http://dx.doi.org/10.1152/jappl.1992.73.3.911.
Повний текст джерелаАнотація:
Twenty sedentary male university students were randomly assigned to an experimental or a control group. The experimental group trained the knee extensors of one leg by producing 30 isometric extension maximal voluntary contractions (MVC) per day, three times per week for 8 wk. After 8 wk of training, extensor MVC in the trained leg increased 32.8% (P less than 0.05), but there was no change in vastus lateralis maximal integrated electromyographic activity (IEMGmax). The most important finding was that the degree of hamstring coactivation during extension MVC decreased by approximately 20% (P less than 0.05) after the 1st wk of training. Less pronounced adaptations occurred in the untrained leg: extension MVC force increased 16.2% (P less than 0.05), hamstring coactivity decreased 13% (P less than 0.05) after 2 wk of training, and vastus lateralis IEMGmax was unchanged. The same measures in legs of the control group were not changed during the study. There were no changes in flexion MVC, biceps femoris IEMGmax, or the degree of quadriceps coactivity during flexion MVC in either leg of the control or experimental group. A reduction in hamstring coactivity in the trained and untrained legs indicates that these muscles provide less opposing force to the contracting quadriceps. We conclude that this small but significant decrease in hamstring coactivation that occurs during the early stages of training is a nonhypertrophic adaptation of the neuromuscular system in response to static resistance training of this type.
10
Kawada, Toru, Shuji Shimizu, Atsunori Kamiya, Yusuke Sata, Kazunori Uemura, and Masaru Sugimachi. "Dynamic characteristics of baroreflex neural and peripheral arcs are preserved in spontaneously hypertensive rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 300, no. 1 (January 2011): R155—R165. http://dx.doi.org/10.1152/ajpregu.00540.2010.
Повний текст джерелаАнотація:
Although baroreceptors are known to reset to operate in a higher pressure range in spontaneously hypertensive rats (SHR), the total profile of dynamic arterial pressure (AP) regulation remains to be clarified. We estimated open-loop transfer functions of the carotid sinus baroreflex in SHR and Wistar Kyoto (WKY) rats. Mean input pressures were set at 120 (WKY120 and SHR120) and 160 mmHg (SHR160). The neural arc transfer function from carotid sinus pressure to efferent splanchnic sympathetic nerve activity (SNA) revealed derivative characteristics in both WKY and SHR. The slope of dynamic gain (in decibels per decade) between 0.1 and 1 Hz was not different between WKY120 (10.1 ± 1.0) and SHR120 (10.4 ± 1.1) but was significantly greater in SHR160 (13.2 ± 0.8, P < 0.05 with Bonferroni correction) than in SHR120. The peripheral arc transfer function from SNA to AP showed low-pass characteristics. The slope of dynamic gain (in decibels per decade) did not differ between WKY120 (−34.0 ± 1.2) and SHR120 (−31.4 ± 1.0) or between SHR120 and SHR160 (−32.8 ± 1.3). The total baroreflex showed low-pass characteristics and the dynamic gain at 0.01 Hz did not differ between WKY120 (0.91 ± 0.08) and SHR120 (0.84 ± 0.13) or between SHR120 and SHR160 (0.83 ± 0.11). In both WKY and SHR, the declining slope of dynamic gain was significantly gentler for the total baroreflex than for the peripheral arc, suggesting improved dynamic AP response in the total baroreflex. In conclusion, the dynamic characteristics of AP regulation by the carotid sinus baroreflex were well preserved in SHR despite significantly higher mean AP.
11
Leikauf, G. D., L. M. Leming, J. R. O'Donnell, and C. A. Doupnik. "Bronchial responsiveness and inflammation in guinea pigs exposed to acrolein." Journal of Applied Physiology 66, no. 1 (January 1, 1989): 171–78. http://dx.doi.org/10.1152/jappl.1989.66.1.171.
Повний текст джерелаАнотація:
Bronchial hyperresponsiveness can be produced experimentally after inhalation of numerous nonimmunospecific stimuli; our objective was to determine whether acrolein, a component of cigarette smoke, could increase bronchial reactivity to intravenously administered acetylcholine in guinea pigs. Bronchial responsiveness was assessed twice before and 1, 2, 6, and 24 h after exposures to less than or equal to 0.01 (sham), 0.31, 0.67, 0.94, or 1.26 parts per million for 2 h (5–7 guinea pigs/group). To examine the possible relationships of responsiveness to inflammatory mediator release and cellular infiltration, bronchoalveolar lavage was performed in another 30 guinea pigs before (control) and 0, 1, 2, 6, or 24 h after exposures. Pulmonary resistance was increased immediately after exposure (5 min) and returned to control values within 30–60 min. Increased bronchial responsiveness was evident within 1 h and became maximal 2–4 h after exposure. The acetylcholine dose necessary to double resistance decreased from 104.2 +/- 7.3 to 79.6 +/- 15.9 at 1 h and was 32.5 +/- 7.9 at 2 h and 32.8 +/- 7.6 micrograms.kg-1 at 6 h. Increases in two eicosanoids, thromboxane B2 (from 167 +/- 21 to 314 +/- 77 pg/ml) and prostaglandin F2 alpha (from 98 +/- 20 to 285 +/- 62 pg/ml) occurred immediately after exposure, whereas an influx of neutrophils occurred 24 h later (from 2.2 +/- 1.2 to 11.3 +/- 3.6%). These temporal relationships suggest that neutrophil infiltration may be a sufficient but not a necessary condition for the onset of bronchial hyperresponsiveness and that injury to cells normally present in the lung are responsible for the mediators thought to influence bronchial responsiveness.
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Starling, Raymond D., Todd A. Trappe, Allen C. Parcell, Chad G. Kerr, William J. Fink, and David L. Costill. "Effects of diet on muscle triglyceride and endurance performance." Journal of Applied Physiology 82, no. 4 (April 1, 1997): 1185–89. http://dx.doi.org/10.1152/jappl.1997.82.4.1185.
Повний текст джерелаАнотація:
Starling, Raymond D., Todd A. Trappe, Allen C. Parcell, Chad G. Kerr, William J. Fink, and David L. Costill. Effects of diet on muscle triglyceride and endurance performance. J. Appl. Physiol. 82(4): 1185–1189, 1997.—The purpose of this investigation was to examine the effects of diet on muscle triglyceride and endurance performance. Seven endurance-trained men completed a 120-min cycling bout at 65% of maximal oxygen uptake. Each subject then ingested an isocaloric high-carbohydrate (Hi-CHO; 83% of energy) or a high-fat (Hi-Fat; 68% of energy) diet for the ensuing 12 h. After a 12-h overnight fast, a 1,600-kJ self-paced cycling bout was completed. Muscle triglyceride measured before (33.0 ± 2.3 vs. 37.0 ± 2.1 mmol/kg dry wt) and after (30.9 ± 2.4 vs. 32.8 ± 1.6 mmol/kg dry wt) the 120-min cycling bout was not different between the Hi-CHO and Hi-Fat trials, respectively. After the 24-h dietary-fasting period, muscle triglyceride was significantly higher for the Hi-Fat (44.7 ± 2.4 mmol/kg dry wt) vs. the Hi-CHO (27.5 ± 2.1 mmol/kg dry wt) trial. Furthermore, self-paced cycling time was significantly greater for the Hi-Fat (139.3 ± 7.1 min) compared with the Hi-CHO (117.1 ± 3.2 min) trial. These data demonstrate that there was not a significant difference in muscle triglyceride concentration before and after a prolonged moderate-intensity cycling bout. Nevertheless, a high-fat diet increased muscle triglyceride concentration and reduced self-paced cycling performance 24 h after the exercise compared with a high-carbohydrate diet.
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Hampson, N. B., E. M. Camporesi, B. W. Stolp, R. E. Moon, J. E. Shook, J. A. Griebel, and C. A. Piantadosi. "Cerebral oxygen availability by NIR spectroscopy during transient hypoxia in humans." Journal of Applied Physiology 69, no. 3 (September 1, 1990): 907–13. http://dx.doi.org/10.1152/jappl.1990.69.3.907.
Повний текст джерелаАнотація:
The effects of mild hypoxia on brain oxyhemoglobin, cytochrome a,a3 redox status, and cerebral blood volume were studied using near-infrared spectroscopy in eight healthy volunteers. Incremental hypoxia reaching 70% arterial O2 saturation was produced in normocapnia [end-tidal PCO2 (PETCO2) 36.9 +/- 2.6 to 34.9 +/- 3.4 Torr] or hypocapnia (PETCO2 32.8 +/- 0.6 to 23.7 +/- 0.6 Torr) by an 8-min rebreathing technique and regulation of inspired CO2. Normocapnic hypoxia was characterized by progressive reductions in arterial PO2 (PaO2, 89.1 +/- 3.5 to 34.1 +/- 0.1 Torr) with stable PETCO2, arterial PCO2 (PaCO2), and arterial pH and resulted in increases in heart rate (35%) systolic blood pressure (14%), and minute ventilation (5-fold). Hypocapnic hypoxia resulted in progressively decreasing PaO2 (100.2 +/- 3.6 to 28.9 +/- 0.1 Torr), with progressive reduction in PaCO2 (39.0 +/- 1.6 to 27.3 +/- 1.9 Torr), and an increase in arterial pH (7.41 +/- 0.02 to 7.53 +/- 0.03), heart rate (61%), and ventilation (3-fold). In the brain, hypoxia resulted in a steady decline of cerebral oxyhemoglobin content and a decrease in oxidized cytochrome a,a3. Significantly greater loss of oxidized cytochrome a,a3 occurred for a given decrease in oxyhemoglobin during hypocapnic hypoxia relative to normocapnic hypoxia. Total blood volume response during hypoxia also was significantly attenuated by hypocapnia, because the increase in volume was only half that of normocapnic subjects. We conclude that cytochrome a,a3 oxidation level in vivo decreases at mild levels of hypoxia. PaCO is an important determinant of brain oxygenation, because it modulates ventilatory, cardiovascular, and cerebral O2 delivery responses to hypoxia.
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Kuhlenhoelter, Alisha M., Kyoungrae Kim, Dustin Neff, Yaohui Nie, A. Nicole Blaize, Brett J. Wong, Shihuan Kuang, et al. "Heat therapy promotes the expression of angiogenic regulators in human skeletal muscle." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 311, no. 2 (August 1, 2016): R377—R391. http://dx.doi.org/10.1152/ajpregu.00134.2016.
Повний текст джерелаАнотація:
Heat therapy has been shown to promote capillary growth in skeletal muscle and in the heart in several animal models, but the effects of this therapy on angiogenic signaling in humans are unknown. We evaluated the acute effect of lower body heating (LBH) and unilateral thigh heating (TH) on the expression of angiogenic regulators and heat shock proteins (HSPs) in healthy young individuals. Exposure to LBH ( n = 18) increased core temperature (Tc) from 36.9 ± 0.1 to 37.4 ± 0.1°C ( P < 0.01) and average leg skin temperature (Tleg) from 33.1 ± 0.1 to 39.6 ± 0.1°C ( P < 0.01), but did not alter the levels of circulating angiogenic cytokines and bone marrow-derived proangiogenic cells (CD34+CD133+). In skeletal muscle, the change in mRNA expression from baseline of vascular endothelial growth factor (VEGF), angiopoietin 2 (ANGPT2), chemokines CCL2 and CX3CL1, platelet factor-4 (PF4), and several members of the HSP family was higher 30 min after the intervention in the individuals exposed to LBH ( n = 11) compared with the control group ( n = 12). LBH also reduced the expression of transcription factor FOXO1 ( P = 0.03). Exposure to TH ( n = 14) increased Tlegfrom 32.8 ± 0.2 to 40.3 ± 0.1°C ( P < 0.05) but Tcremained unaltered (36.8 ± 0.1°C at baseline and 36.9 ± 0.1°C at 90 min). This intervention upregulated the expression of VEGF, ANGPT1, ANGPT2, CCL2, and HSPs in skeletal muscle but did not affect the levels of CX3CL1, FOXO-1, and PF4. These findings suggest that both LBH and TH increase the expression of factors associated with capillary growth in human skeletal muscle.
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Masa, Juan F., Jaime Corral, Julio Sanchez de Cos, Joaquin Duran-Cantolla, Marta Cabello, Luis Hernández-Blasco, Carmen Monasterio, et al. "Effectiveness of Three Sleep Apnea Management Alternatives." Sleep 36, no. 12 (December 1, 2013): 1799–807. http://dx.doi.org/10.5665/sleep.3204.
Повний текст джерела
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Barak, Otto F., Kresimir Caljkusic, Ryan L. Hoiland, Philip N. Ainslie, Stephen R. Thom, Ming Yang, Pavle Jovanov, and Zeljko Dujic. "Differential influence of vitamin C on the peripheral and cerebral circulation after diving and exposure to hyperoxia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 315, no. 4 (October 1, 2018): R759—R767. http://dx.doi.org/10.1152/ajpregu.00412.2017.
Повний текст джерелаАнотація:
We examined if the diving-induced vascular changes in the peripheral and cerebral circulation could be prevented by oral antioxidant supplementation. Fourteen divers performed a single scuba dive to eighteen meter sea water for 47 min. Twelve of the divers participated in a follow-up study involving breathing 60% of oxygen at ambient pressure for 47 min. Before both studies, participants ingested vitamin C (2 g/day) or a placebo capsule for 6 days. After a 2-wk washout, the study was repeated with the different condition. Endothelium-dependent vasodilator function of the brachial artery was assessed pre- and postintervention using the flow-mediated dilation (FMD) technique. Transcranial Doppler ultrasound was used to measure intracranial blood velocities pre- and 90 min postintervention. FMD was reduced by ∼32.8% and ∼21.2% postdive in the placebo and vitamin C trial and posthyperoxic condition in the placebo trial by ∼28.2% ( P < 0.05). This reduction in FMD was attenuated by ∼10% following vitamin C supplementation in the hyperoxic study ( P > 0.05). Elevations in intracranial blood velocities 30 min after surfacing from diving were reduced in the vitamin C study compared with the placebo trial ( P < 0.05). O2 breathing had no postintervention effects on intracranial velocities ( P > 0.05). Prophylactic ingestion of vitamin C effectively abrogated peripheral vascular dysfunction following exposure to 60% O2 but did not abolish the postdive decrease in FMD. Transient elevations of intracranial velocities postdive were reduced by vitamin C. These findings highlight the differential influence of vitamin C on peripheral and cerebral circulations following scuba diving, which are only partly mediated via hyperoxia.
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Mack, G. W., L. M. Shannon, and E. R. Nadel. "Influence of beta-adrenergic blockade on the control of sweating in humans." Journal of Applied Physiology 61, no. 5 (November 1, 1986): 1701–5. http://dx.doi.org/10.1152/jappl.1986.61.5.1701.
Повний текст джерелаАнотація:
To evaluate the role of beta-adrenergic receptors in the control of human sweating, we studied six subjects during 40 min of cycle-ergometer exercise (60% maximal O2 consumption) at 22 degrees C 2 h after oral administration of placebo or nonselective beta-blockade (BB, 80 mg propranolol). Internal temperature (esophageal temperature, Tes), mean skin temperature (Tsk), local chest temperature (Tch), and local chest sweat rate (msw) were continuously recorded. The control of sweating was best described by the slope of the linear relationship between msw and Tes and the threshold Tes for the onset of sweating. The slope of the msw-Tes relationship decreased 27% (P less than 0.01), from 1.80 to 1.30 mg X cm-2 X min-1 X degree C-1 during BB. The Tes threshold for sweating (36.8 degrees C) was not altered as the result of BB. These data suggest that BB modified the control of sweating via some peripheral interaction. Since Tsk was significantly (P less than 0.05) reduced during BB exercise, from a control value of 32.8 to 32.2 degrees C, we evaluated the influence of the reduction in local skin temperature (Tsk) in the altered control of sweating. Reductions in Tch accounted for only 45% of the decrease in the slope of the msw-Tes relationship during BB. Since evaporative heat loss requirement during exercise with BB, as estimated from the energy balance equation, was also reduced 18%, compared with control exercise, we concluded that during BB the reduction in sweating at any Tes is the consequence of both a decrease in local Tsk and a direct effect on sweat gland.
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Shido, O., Y. Yoneda, and T. Nagasaka. "Changes in body temperature of rats acclimated to heat with different acclimation schedules." Journal of Applied Physiology 67, no. 5 (November 1, 1989): 2154–57. http://dx.doi.org/10.1152/jappl.1989.67.5.2154.
Повний текст джерелаАнотація:
Male Wistar rats, initially maintained at an ambient temperature (Ta) of 23.8 degrees C, were subjected to one of seven different heat acclimation schedules under a 12:12-h light-dark cycle (lights on at 0600 h). Two groups of rats were exposed to Ta of 32.4 degrees C all day for 5 (HC5) or 10 (HC10) days. The other four groups were exposed to Ta of 32.8 degrees C for 5 h/day during the last half of the dark phase for 5 (NI5) or 10 (NI10) consecutive days or during the last half of the light phase for 5 (DI5) or 10 (DI10) consecutive days. Control rats (C) were kept at 23.8 degrees C throughout the experiment. Hypothalamic temperature (Thy) was measured every 5 min with a chronically implanted thermocouple from 1 day before the beginning to 2 days after the end of the heat acclimation periods. During the heat acclimation periods, daily mean Thy rose significantly in HC5 and HC10 rats but decreased significantly in NI5 and NI10 rats. Daily mean Thy did not change in C, DI5, and DI10 rats. Thy in HC10 rats sharply decreased at the end of the heat acclimation periods and remained at low levels for approximately 3 h. On the 2nd postacclimation day, however, mean Thy returned and remained at a significantly higher level. In NI10 rats, the mean Thy in the postacclimation period was significantly lower than the preacclimation values. No such changes in mean Thy were observed in DI10 rats. Five-days of heat exposure had little effect on the postacclimation Thy.(ABSTRACT TRUNCATED AT 250 WORDS)
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Shido, O., and T. Nagasaka. "Thermoregulatory responses to acute body heating in rats acclimated to continuous heat exposure." Journal of Applied Physiology 68, no. 1 (January 1, 1990): 59–65. http://dx.doi.org/10.1152/jappl.1990.68.1.59.
Повний текст джерелаАнотація:
Thermoregulatory responses to an acute heat load with intraperitoneal heating (IH) or indirect external warming (EW) by increasing ambient temperature (Ta) were investigated with direct and indirect calorimetry in rats acclimated to environments of 24.0 degrees C (Cn), 29.4 degrees C (H1), and 32.8 degrees C (H2) for greater than 15 days. The rats were placed in a direct calorimeter where the air temperature was maintained at 24 degrees C for the initial 3 h. IH was then made for 30 min through an electric heater implanted chronically (6.5 W.kg-1) in the peritoneal cavity, and EW was performed by raising the jacket water temperature surrounding the calorimeter from 24 to 39 degrees C (0.19 degrees C.min-1). Hypothalamic (Thy) and colonic temperature immediately before the start of the heat load tended to be higher as the acclimation temperature increased. During IH, the threshold Thy for the tail skin vasodilation (Tth) was significantly higher in H2 than in Cn rats. During EW, however, there was no difference in Tth between the groups. Metabolic heat production (M) was slightly suppressed during IH and significantly depressed only in H2 rats. During EW, M was suppressed in all the groups. The magnitude and duration of suppression were greater in H2 rats than in the other two groups. The responses in nonevaporative heat loss and thermal conductance (C) to the rise in Thy did not differ among the three groups during IH. According to the rise in Thy, however, there was a greater C increase in H2 than in Cn and H1 rats during EW.(ABSTRACT TRUNCATED AT 250 WORDS)
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Moir, Hannah, Michael G. Hughes, Stephen Potter, Craig Sims, Lee R. Butcher, Nia A. Davies, Kenneth Verheggen, Kenneth P. Jones, Andrew W. Thomas, and Richard Webb. "Exercise-induced immunosuppression: roles of reactive oxygen species and 5′-AMP-activated protein kinase dephosphorylation within immune cells." Journal of Applied Physiology 108, no. 5 (May 2010): 1284–92. http://dx.doi.org/10.1152/japplphysiol.00737.2009.
Повний текст джерелаАнотація:
We previously proposed 5′-AMP-activated protein kinase (AMPK) dephosphorylation within immune cells as an intracellular mechanism linking exercise and immunosuppression. In this study, AMPK phosphorylation underwent transient (<1 h) decreases (53.8 ± 7.2% basal) immediately after exercise (45 min of cycling at 70% V̇o2max) in a cohort of 16 adult male participants. Similar effects were seen with running. However, because exercise-induced inactivation of AMPK was previously shown to occur in an AMP-independent manner, the means by which AMPK is inactivated in this context is not yet clear. To investigate the hypothesis that exercise-induced inactivation of AMPK is mediated via signaling mechanisms distinct from changes in cellular AMP-to-ATP ratios, reactive oxygen species (ROS) and intracellular Ca2+ signaling were investigated in mononuclear cells before and after exercise and in cultured monocytic MM6 cells. In in vitro studies, treatment with an antioxidant (ascorbic acid, 4 h, 50 μM) decreased MM6 cell intracellular ROS levels (88.0 ± 5.2% basal) and induced dephosphorylation of AMPK (44.7 ± 17.6% basal). By analogy, the fact that exercise decreased mononuclear cell ROS content (32.8 ± 16.6% basal), possibly due to downregulation (43.4 ± 8.0% basal) of mRNA for NOX2, the catalytic subunit of the cytoplasmic ROS-generating enzyme NADPH oxidase, may provide an explanation for the AMPK-dephosphorylating effect of exercise. In contrast, exercise-induced Ca2+ signaling events did not seem to be coupled to changes in AMPK activity. Thus we propose that the exercise-induced decreases in both intracellular ROS and AMPK phosphorylation seen in this study constitute evidence supporting a role for ROS in controlling AMPK, and hence immune function, in the context of exercise-induced immunosuppression.
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Spencer, T. N., K. J. Botting, J. L. Morrison, and G. S. Posterino. "Contractile and Ca2+-handling properties of the right ventricular papillary muscle in the late-gestation sheep fetus." Journal of Applied Physiology 101, no. 3 (September 2006): 728–33. http://dx.doi.org/10.1152/japplphysiol.00214.2006.
Повний текст джерелаАнотація:
The force-generating capacity of cardiomyocytes rapidly changes during gestation and early postnatal life coinciding with a transition in cardiomyocyte nucleation in both mice and rats. Changes in nucleation, in turn, appear to coincide with important changes in the excitation-contraction coupling architecture. However, it is not clear whether similar changes are observed in other mammals in which this transition occurs prenatally, such as sheep. Using small (70–300 μM diameter) chemically skinned cardiomyocyte bundles from the right ventricular papillary muscle of sheep fetuses at 126–132 and 137–140 days (d) gestational age (GA), we aimed to examine whether changes in cardiomyocyte nucleation during late gestation coincided with developmental changes in excitation-contraction coupling parameters (e.g., Ca2+ uptake, Ca2+ release, and force development). All experiments were conducted at room temperature (23 ± 1°C). We found that the proportion of mononucleate cardiomyocytes decreased significantly with GA (126–132d, 45.7 ± 4.7%, n = 7; 137–140d, 32.8 ± 1.6%, n = 6; P < 0.05). When we then examined force development between the two groups, there was no significant difference in either the maximal Ca2+-activated force (6.73 ± 1.54 mN/mm2, n = 14 vs. 6.55 ± 1.25 mN/mm2, n = 7, respectively) or the Ca2+ sensitivity of the contractile apparatus (pCa at 50% maximum Ca2+-activated force: 126–132d, 6.17 ± 0.06, n = 14; 137–140d, 6.24 ± 0.08, n = 7). However, sarcoplasmic reticulum (SR) Ca2+ uptake rates (but not Ca2+ release) increased with GA ( P < 0.05). These data reveal that during late gestation in sheep when there is a major transition in cardiomyocyte nucleation, SR Ca2+ uptake rates increase, which would influence total SR Ca2+ content and force production.
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Convertino, Victor A. "Mechanisms of blood pressure regulation that differ in men repeatedly exposed to high-G acceleration." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 4 (April 1, 2001): R947—R958. http://dx.doi.org/10.1152/ajpregu.2001.280.4.r947.
Повний текст джерелаАнотація:
The purpose of this study was to test the hypothesis that repeated exposure to high acceleration (G) would be associated with enhanced functions of specific mechanisms of blood pressure regulation. We measured heart rate (HR), stroke volume (SV), cardiac output (Q̊), mean arterial blood pressure, central venous pressure, forearm and leg vascular resistance, catecholamines, and changes in leg volume (%ΔLV) during various protocols of lower body negative pressure (LBNP), carotid stimulation, and infusions of adrenoreceptor agonists in 10 males after three training sessions on different days over a period of 5–7 days using a human centrifuge (G trained). These responses were compared with the same measurements in 10 males who were matched for height, weight, and fitness but did not undergo G training (controls). Compared with the control group, G-trained subjects demonstrated greater R-R interval response to equal carotid baroreceptor stimulation (7.3 ± 1.2 vs. 3.9 ± 0.4 ms/mmHg, P = 0.02), less vasoconstriction to equal low-pressure baroreceptor stimulation (−1.4 ± 0.2 vs. −2.6 ± 0.3 U/mmHg, P = 0.01), and higher HR (−1.2 ± 0.2 vs. −0.5 ± 0.1 beats · min−1 · mmHg−1, P = 0.01) and α-adrenoreceptor response (32.8 ± 3.4 vs. 19.5 ± 4.7 U/mmHg, P = 0.04) to equal dose of phenylephrine. During graded LBNP, G-trained subjects had less decline in Q̊ and SV, %ΔLV, and elevation in thoracic impedance. G-trained subjects also had greater total blood (6,497 ± 496 vs. 5,438 ± 228 ml, P = 0.07) and erythrocyte (3,110 ± 364 vs. 2,310 ± 96 ml, P = 0.06) volumes. These results support the hypothesis that exposure to repeated high G is associated with increased capacities of mechanisms that underlie blood pressure regulation.
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Howlett, Richard A., Casey A. Kindig, and Michael C. Hogan. "Intracellular Po2 kinetics at different contraction frequencies in Xenopus single skeletal muscle fibers." Journal of Applied Physiology 102, no. 4 (April 2007): 1456–61. http://dx.doi.org/10.1152/japplphysiol.00422.2006.
Повний текст джерелаАнотація:
Increasing contraction frequency in single skeletal muscle fibers has been shown to increase the magnitude of the fall in intracellular Po2 (PiO2), reflecting a greater metabolic rate. To test whether PiO2 kinetics are altered by contraction frequency through this increase in metabolic stress, PiO2 was measured in Xenopus single fibers ( n = 11) during and after contraction bouts at three different frequencies. PiO2 was measured via phosphorescence quenching at 0.16-, 0.25-, and 0.5-Hz tetanic stimulation. The kinetics of the change in PiO2 from resting baseline to end-contraction values and end contraction to rest were described as a mean response time (MRT) representing the time to 63% of the change in PiO2. As predicted, the fall in PiO2 from baseline following contractions was progressively greater at 0.5 and 0.25 Hz than at 0.16 Hz (32.8 ± 2.1 and 29.3 ± 2.0 Torr vs. 23.6 ± 2.2 Torr, respectively) since metabolic demand was greater. The MRT for the decrease in PiO2 was progressively faster at the higher frequencies (0.5 Hz: 45.3 ± 4.5 s; 0.25 Hz: 63.3 ± 4.1 s; 0.16 Hz: 78.0 ± 4.1 s), suggesting faster accumulation of stimulators of oxidative phosphorylation. The MRT for PiO2 off-kinetics (0.5 Hz: 84.0 ± 11.7 s; 0.25 Hz: 79.1 ± 8.4 s; 0.16 Hz: 81.1 ± 8.3 s) was not different between trials. These data demonstrate in single fibers that the rate of the fall in PiO2 is dependent on contraction frequency, whereas the rate of recovery following contractions is independent of either the magnitude of the fall in PiO2 from baseline or the contraction frequency. This suggests that stimulation frequency plays an integral role in setting the initial metabolic response to work in isolated muscle fibers, possibly due to temporal recovery between contractions, but it does not determine recovery kinetics.
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Heusser, Karsten, Gordan Dzamonja, Toni Breskovic, Craig D. Steinback, André Diedrich, Jens Tank, Jens Jordan, and Zeljko Dujic. "Sympathetic and cardiovascular responses to glossopharyngeal insufflation in trained apnea divers." Journal of Applied Physiology 109, no. 6 (December 2010): 1728–35. http://dx.doi.org/10.1152/japplphysiol.00522.2010.
Повний текст джерелаАнотація:
Glossopharyngeal insufflation (lung packing) is a common maneuver among experienced apnea divers by which additional air is pumped into the lungs. It has been shown that packing may compromise cardiovascular homeostasis. We tested the hypothesis that the packing-mediated increase in intrathoracic pressure enhances the baroreflex-mediated increase in muscle sympathetic nerve activity (MSNA) in response to an exaggerated drop in cardiac output (CO). We compared changes in hemodynamics and MSNA (peroneal microneurography) during maximal breath-holds without and with prior moderate packing (0.79 ± 0.40 liters) in 14 trained divers (12 men, 2 women, 26.7 ± 4.5 yr, body mass index 24.8 ± 2.4 kg/m2). Packing did not change apnea time (3.8 ± 1.0 vs. 3.8 ± 1.2 min), hemoglobin oxygen desaturation (−17.6 ± 12.3 vs. −18.7 ± 12.8%), or the reduction in CO (1 min: −3.65 ± 1.83 vs. −3.39 ± 1.96 l/min; end of apnea: −2.44 ± 1.33 vs. −2.16 ± 1.44 l/min). On the other hand, packing dampened the early, i.e., 1-min increase in mean arterial pressure (MAP, 1 min: 9.2 ± 8.3 vs. 2.4 ± 11.0 mmHg, P < 0.01) and in total peripheral resistance (relative TPR, 1 min: 2.1 ± 0.5 vs. 1.9 ± 0.5, P < 0.05) but it augmented the concomitant rise in MSNA (1 min: 28.0 ± 11.7 vs. 39.4 ± 12.7 bursts/min, P < 0.001; 32.8 ± 16.4 vs. 43.9 ± 14.8 bursts/100 heart beats, P < 0.01; 3.3 ± 2.1 vs. 4.8 ± 3.2 au/min, P < 0.05). We conclude that the early sympathoactivation 1 min into apnea after moderate packing is due to mechanisms other than excessive reduction in CO. We speculate that lower MAP despite increased MSNA after packing might be explained by vasodilator substances released by the lungs. This idea should be addressed in future studies.
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Stachenfeld, Nina S., and Hugh S. Taylor. "Sex hormone effects on body fluid and sodium regulation in women with and without exercise-associated hyponatremia." Journal of Applied Physiology 107, no. 3 (September 2009): 864–72. http://dx.doi.org/10.1152/japplphysiol.91211.2008.
Повний текст джерелаАнотація:
We hypothesized that exercise-associated hyponatremia (EAH) is a function of excess sodium loss combined with high water intake in women at risk for dysnatremias during endurance exercise. We further hypothesized that estradiol and progesterone exposure increases fluid retention and sodium loss during exercise in women at risk for EAH. For 16 days we suppressed estrogens and progesterone with a gonadotropin-releasing hormone antagonist (GnRH ant) in seven women with (Hypo) and nine women without (no Hypo) a history of hyponatremia; we added 17β-estradiol (0.2 mg/day patches) for days 4–16 (E2) and progesterone (200 mg/day) for days 13–16 (E2-P4). Under each hormone condition, subjects cycled in 35°C at 65% peak oxygen consumption (V̇o2peak) for 60 min, then at 55–60% V̇o2peak for 120 min. Subjects drank 8 ml/kg of water (and replenished urine volume) every 30 min over the final 120 min of exercise. S[Na+] fell by 4.3, 3.9, and 3.1 meq/l ( P < 0.05) with drinking during GnRH ant, E2, and E2-P4 in Hypo, with little fall in no Hypo. Under all conditions, combined urine and sweat sodium loss were similar between Hypo [−85.6 (SD 36.2), −86.4 (SD 39.2), and −112.0 (SD 30.0) meq] and no Hypo [−98.0 (SD 54.8), −80.9 (SD 57.6), and −105.1 (SD 46.4) meq, for GnRH, E2, and E2-P4], as was mass balance of electrolytes (EMB) for Hypo [−104.8 (SD 32.8), −103.6 (SD 42.1), and −132.8 (SD 34.9) meq] compared with no Hypo [−128.8 (SD 57.2), −113.5 (SD 61.1), and −143.4 (SD 49.6) meq for GnRH, E2, and E2-P4]. Mass balance of water [VMB, for Hypo, 0.42 (SD 0.10), 0.62 (SD 0.25), and −0.11 (SD 0.11) liter] compared with no Hypo [0.01 (SD 0.15), 0.03 (SD 17), and −0.16 (SD 0.13) liter for GnRH, E2, and E2-P4, P < 0.05] indicates water retention was the primary contributor to the lower S[Na+] in Hypo women.
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Fu, Z., M. L. Costello, K. Tsukimoto, R. Prediletto, A. R. Elliott, O. Mathieu-Costello, and J. B. West. "High lung volume increases stress failure in pulmonary capillaries." Journal of Applied Physiology 73, no. 1 (July 1, 1992): 123–33. http://dx.doi.org/10.1152/jappl.1992.73.1.123.
Повний текст джерелаАнотація:
We previously showed that when pulmonary capillaries in anesthetized rabbits are exposed to a transmural pressure (Ptm) of approximately 40 mmHg, stress failure of the walls occurs with disruption of the capillary endothelium, alveolar epithelium, or sometimes all layers. The present study was designed to test whether stress failure occurred more frequently at high than at low lung volumes for the same Ptm. Lungs of anesthetized rabbits were inflated to a transpulmonary pressure of 20 cmH2O, perfused with autologous blood at 32.5 or 2.5 cmH2O Ptm, and fixed by intravascular perfusion. Samples were examined by both transmission and scanning electron microscopy. The results were compared with those of a previous study in which the lung was inflated to a transpulmonary pressure of 5 cmH2O. There was a large increase in the frequency of stress failure of the capillary walls at the higher lung volume. For example, at 32.5 cmH2O Ptm, the number of endothelial breaks per millimeter cell lining was 7.1 +/- 2.2 at the high lung volume compared with 0.7 +/- 0.4 at the low lung volume. The corresponding values for epithelium were 8.5 +/- 1.6 and 0.9 +/- 0.6. Both differences were significant (P less than 0.05). At 52.5 cmH2O Ptm, the results for endothelium were 20.7 +/- 7.6 (high volume) and 7.1 +/- 2.1 (low volume), and the corresponding results for epithelium were 32.8 +/- 11.9 and 11.4 +/- 3.7. At 32.5 cmH2O Ptm, the thickness of the blood-gas barrier was greater at the higher lung volume, consistent with the development of more interstitial edema. Ballooning of the epithelium caused by accumulation of edema fluid between the epithelial cell and its basement membrane was seen at 32.5 and 52.5 cmH2O Ptm. At high lung volume, the breaks tended to be narrower and fewer were oriented perpendicular to the axis of the pulmonary capillaries than at low lung volumes. Transmission and scanning electron microscopy measurements agreed well. Our findings provide a physiological mechanism for other studies showing increased capillary permeability at high states of lung inflation.
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Raj, Rishabh, Uma Devaraj, Chitra Veluthat, Kavitha Venkatnarayan, Priya Ramachandran, and Uma Maheswari Krishnaswamy. "Development of a reference equation for maximal exercise capacity in normal Indian subjects using cardiopulmonary exercise testing." Indian Journal of Physiology and Pharmacology 66 (August 10, 2022): 120–25. http://dx.doi.org/10.25259/ijpp_364_2021.
Повний текст джерелаАнотація:
Objectives: Cardiopulmonary exercise testing (CPET) is an integrative assessment of multiple interdependent variables contributing to exercise response. CPET parameters such as maximum or peak oxygen uptake (VO2max/peak) are used to estimate this response. VO2max/peak varies with physiological predictors such as age, sex, body mass index (BMI), and activity level. The existing normative values for Indian subjects have, thus, far been adapted from Western populations who have a different body habitus in terms of these physiological predictors. We aimed to determine the relation and a prediction equation of these variables with VO2peak. Materials and Method: One hundred and twenty-one healthy subjects underwent CPET on a treadmill (Cortex Metalyzer) in a tertiary care hospital and VO2peak was calculated through Metasoft software. Statistical analysis: Student’s t-test and one-way analysis of variance (ANOVA) were used for calculating the between-group difference. Logistic regression with univariate and multivariate ANOVA was used for computing the reference equation. Results: Mean VO2peak (ml/min/kg) was 29.9 ± 7.7. It was higher for males (32.81 ± 7.9 vs. 26.79 ± 6.1 [P < 0.001]) and active individuals (32.8 ± 7 vs. 26.1 ± 6.9 [P < 0.001]). Higher values were observed in younger and non-obese population (P < 0.001). Regression coefficient (r2) was 0.44 and 0.36 for male and female, respectively. Reference equation was then calculated for males and females using the r2 value. Conclusion: VO2peak was higher in males and active individuals, it declined with increasing age and BMI. The values obtained were much lower than the Western population, therefore stressing the need for the development of our own set of reference equations.
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Granados, Jorge, Trevor L. Gillum, Kevin M. Christmas та Matthew R. Kuennen. "Prohormone supplement 3β-hydroxy-5α-androst-1-en-17-one enhances resistance training gains but impairs user health". Journal of Applied Physiology 116, № 5 (1 березня 2014): 560–69. http://dx.doi.org/10.1152/japplphysiol.00616.2013.
Повний текст джерелаАнотація:
Prohormone supplements (PS) are recognized not to impart anabolic or ergogenic effects in men, but the research supporting these conclusions is dated. The Anabolic Steroid Control Act was amended in 2004 to classify androstenedione and 17 additional anabolic compounds as controlled substances. The viability of PS that entered the market after that time have not been evaluated. Seventeen resistance-trained men (23 ± 1 yr; 13.1 ± 1.5% body fat) were randomly assigned to receive either 330 mg/day of 3β-hydroxy-5α-androst-1-en-17-one (Prohormone; n = 9) or sugar (Placebo; n = 8) per os and complete a 4-wk (16 session) structured resistance-training program. Body composition, muscular strength, circulating lipids, and markers of liver and kidney dysfunction were assessed at study onset and termination. Prohormone increased lean body mass by 6.3 ± 1.2%, decreased fat body mass by 24.6 ± 7.1%, and increased their back squat one repetition maximum and competition total by 14.3 ± 1.5 and 12.8 ± 1.1%, respectively. These improvements exceeded ( P < 0.05) Placebo, which increased lean body mass by 0.5 ± 0.8%, reduced fat body mass by 9.5 ± 3.6%, and increased back squat one repetition maximum and competition total by 5.7 ± 1.7 and 5.9 ± 1.7%, respectively. Prohormone also experienced multiple adverse effects. These included a 38.7 ± 4.0% reduction in HDL ( P < 0.01), a 32.8 ± 15.05% elevation in LDL ( P < 0.01), and elevations of 120.0 ± 22.6 and 77.4 ± 12.0% in LDL-to-HDL and cholesterol-to-HDL ratios, respectively (both P < 0.01). Prohormone also exhibited elevations in serum creatinine (19.6 ± 4.3%; P < 0.01) and aspartate transaminase (113.8 ± 61.1%; P = 0.05), as well as reductions in serum albumin (5.1 ± 1.9%; P = 0.04), alkaline phosphatase (16.4 ± 4.7%; P = 0.04), and glomerular filtration rate (18.0 ± 3.3%; P = 0.04). None of these values changed (all P > 0.05) in Placebo. The oral PS 3β-hydroxy-5α-androst-1-en-17-one improves body composition and muscular strength. However, these changes come at a significant cost. Cardiovascular health and liver function are particularly compromised. Given these findings, we feel the harm associated with this particular PS outweighs any potential benefit.
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Sood, Nilita, Scott E. Turcotte, Nastasia V. Wasilewski, Thomas Fisher, Taylar Wall, John T. Fisher, and M. Diane Lougheed. "Small-airway obstruction, dynamic hyperinflation, and gas trapping despite normal airway sensitivity to methacholine in adults with chronic cough." Journal of Applied Physiology 126, no. 2 (February 1, 2019): 294–304. http://dx.doi.org/10.1152/japplphysiol.00635.2018.
Повний текст джерелаАнотація:
The clinical relevance of cough during methacholine challenge in individuals with normal airway sensitivity is unknown. We compared responses of individuals with chronic cough who cough during high-dose methacholine bronchoprovocation and have normal versus increased airway sensitivity to healthy controls. Fifteen healthy participants (CONTROL) aged 26 ± 7 yr (mean ± SD) and 32 participants aged 42 ± 14 yr with chronic cough and suspected asthma completed high-dose methacholine challenge testing. Three participants who did not cough and had normal airway sensitivity were excluded. Spirometry and lung volumes were compared at the maximum response (MAX) among 1) ASTHMA [ n = 15, provocative concentration of methacholine causing a 20% fall in forced expiratory volume in 1 s (FEV1) from baseline (PC20) 4.71 ± 1.37 mg/ml], 2) methacholine-induced cough with normal airway sensitivity (COUGH, n = 14, PC20 41.2 ± 18.7 mg/ml for 3 participants with a measurable PC20), and 3) CONTROL ( n = 15; PC20 93.4 ± 95.4 mg/ml for 4 participants with a measurable PC20). Esophageal pressure-derived pulmonary mechanics were compared at MAX for the ASTHMA and COUGH groups. From baseline to MAX, FEV1 and forced expiratory flow between 25% and 75% of forced vital capacity decreased more in ASTHMA (−36.2 ± 3.8 %pr; −47.1 ± 6.9 %pr, respectively) than COUGH (−12.2 ± 3.0 %pr ( P < 0.001); −24.7 ± 6.5 %pr ( P < 0.001), respectively) and CONTROL (−13.7 ± 2.0 %pr ( P < 0.001); −32.8 ± 5.4 %pr ( P < 0.017), respectively). In both ASTHMA and COUGH, inspiratory capacity decreased by 500–800 ml, and functional residual capacity and residual volume increased by ~800 ml. Individuals with COUGH develop dynamic hyperinflation and gas trapping comparable to individuals with ASTHMA despite less bronchoconstriction and smaller reductions in mid-to-late expiratory flows, which leads us to believe that COUGH is a distinct phenotype. NEW & NOTEWORTHY Healthy individuals and individuals with chronic cough who demonstrate normal airway sensitivity but cough during methacholine bronchoprovocation bronchoconstrict less than individuals with mild asthma. However, those who cough and have normal airway sensitivity develop dynamic hyperinflation and gas trapping comparable to individuals with mild asthma. Thus, methacholine-induced cough with normal airway sensitivity may be clinically relevant, related to reversible small airway obstruction and preservation of the bronchodilating and/or bronchoprotective effects of deep inspirations.
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Yalçin, Fatih, Nagehan Kucukler, Oscar Cingolani, Blaid Mbiyangandu, Lars Sorensen, Aurelio Pinherio, M. Roselle Abraham, and Theodore P. Abraham. "Evolution of ventricular hypertrophy and myocardial mechanics in physiological and pathological hypertrophy." Journal of Applied Physiology 126, no. 2 (February 1, 2019): 354–62. http://dx.doi.org/10.1152/japplphysiol.00199.2016.
Повний текст джерелаАнотація:
Left ventricular hypertrophy (LVH) is an adaptive response to physiological or pathological stimuli, and distinguishing between the two has obvious clinical implications. However, asymmetric septal hypertrophy and preserved cardiac function are noted in early stages in both cases. We characterized the early anatomic and functional changes in a mouse model of physiological and pathological stress using serial echocardiography-based morphometry and tissue velocity imaging. Weight-matched CF-1 male mice were separated into Controls ( n = 10), treadmill Exercise 1 h daily for 5 days/wk ( n = 7), and transverse aortic constriction (TAC, n = 7). Hypertrophy was noted first in the left ventricle basal septum compared with other segments in Exercise (0.84 ± 0.02 vs. 0.79 ± 0.03 mm, P = 0.03) and TAC (0.86 ± 0.05 vs. 0.77 ± 0.04 mm, P = 0.02) at 4 and 3 wk, respectively. At 8 wk, eccentric LVH was noted in Exercise and concentric LVH in TAC. Septal E/E′ ratio increased in TAC (32.6 ± 3.7 vs. 37 ± 6.2, P = 0.002) compared with the Controls and Exercise (32.3 ± 5.2 vs. 32.8 ± 3.8 and 31.2 ± 4.9 vs. 28.2 ± 5.0, respectively, nonsignificant for both). Septal s′ decreased in TAC (21 ± 3.6 vs. 17 ± 4.2 mm/s, P = 0.04) but increased in Exercise (19.6 ± 4.1 vs. 29.2 ± 2.3 mm/s, P = 0.001) and was unchanged in Controls (20.1 ± 4.2 vs. 20.9 ± 5.1 mm/s, nonsignificant). With similar asymmetric septal hypertrophy and normal global function during the first 4–8 wk of pathological and physiological stress, there is an early marginal increase with subsequent decrease in systolic tissue velocity in pathological but early and progressive increase in physiological hypertrophy. Tissue velocities may help adjudicate between these two states when there are no overt anatomic or functional differences. NEW & NOTEWORTHY Pathological and physiological stress-induced ventricular hypertrophy have different clinical connotations but present with asymmetric septal hypertrophy and normal global function in their early stages. We observed a marginal but statistically significant decrease in systolic tissue velocity in pathological but progressive increase in velocity in physiological hypertrophy. Tissue velocity imaging could be an important tool in the management of asymmetric septal hypertrophy by adjudicating between these two etiologies when there are no overt anatomic or functional differences.
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Song, Daisheng, Keith A. Sharkey, Deanne R. Breitman, Yikun Zhang, and Samuel S. Lee. "Disordered central cardiovascular regulation in portal hypertensive and cirrhotic rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 3 (March 1, 2001): G420—G430. http://dx.doi.org/10.1152/ajpgi.2001.280.3.g420.
Повний текст джерелаАнотація:
Portal hypertension due to either prehepatic portal hypertension or cirrhosis is associated with cardiovascular derangement. We aimed to delineate regulatory mechanisms in the brain stem cardiovascular nuclei in rat models of prehepatic portal hypertension and cirrhosis. Neuronal activation in the nucleus of the solitary tract (NTS) and ventrolateral medulla (VLM) were assessed by immunohistochemical staining for the immediate-early gene product Fos. In the same sections, catecholaminergic neurons were counted by tyrosine hydroxylase (TH) staining. Ninety minutes after hypotensive hemorrhage (or no volume challenge), the animals were killed for Fos and TH medullary staining. These protocols were repeated after capsaicin administration. The NTS of unchallenged sham-operated rats had scant Fos-positive cells (3.6 ± 0.4 cells/section), whereas hemorrhage significantly increased Fos staining (91.8 ± 14). In contrast, the unchallenged portal hypertensive and cirrhotic groups showed increased Fos staining (14.3 ± 5.8 and 32.8 ± 2.8, respectively), which hemorrhage did not alter significantly. The numbers of TH-positive cells were similar in the three unchallenged groups; double labeling revealed that ∼50% of TH-positive cells were activated by hemorrhage in the sham and cirrhotic rats but not the portal hypertensive rats. Similar patterns of Fos and TH staining were observed in the VLM. Capsaicin treatment not only significantly reduced the Fos-positive neuron numbers in portal hypertensive and cirrhotic rats but also attenuated hemorrhage-induced Fos and double-positive cells in both NTS and VLM. These results suggest that disordered trafficking in capsaicin-sensitive nerves and central dysregulation contribute to blunted cardiovascular responsiveness in cirrhosis and prehepatic portal hypertension.
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O'Grady, Gregory, Peng Du, Wim J. E. P. Lammers, John U. Egbuji, Pulasthi Mithraratne, Jiande D. Z. Chen, Leo K. Cheng, John A. Windsor, and Andrew J. Pullan. "High-resolution entrainment mapping of gastric pacing: a new analytical tool." American Journal of Physiology-Gastrointestinal and Liver Physiology 298, no. 2 (February 2010): G314—G321. http://dx.doi.org/10.1152/ajpgi.00389.2009.
Повний текст джерелаАнотація:
Gastric pacing has been investigated as a potential treatment for gastroparesis. New pacing protocols are required to improve symptom and motility outcomes; however, research progress has been constrained by a limited understanding of the effects of electrical stimulation on slow-wave activity. This study introduces high-resolution (HR) “entrainment mapping” for the analysis of gastric pacing and presents four demonstrations. Gastric pacing was initiated in a porcine model (typical amplitude 4 mA, pulse width 400 ms, period 17 s). Entrainment mapping was performed using flexible multielectrode arrays (≤192 electrodes; 92 cm2) and was analyzed using novel software methods. In the first demonstration, entrainment onset was quantified over successive waves in spatiotemporal detail. In the second demonstration, slow-wave velocity was accurately determined with HR field analysis, and paced propagation was found to be anisotropic (longitudinal 2.6 ± 1.7 vs. circumferential 4.5 ± 0.6 mm/s; P < 0.001). In the third demonstration, a dysrhythmic episode that occurred during pacing was mapped in HR, revealing an ectopic slow-wave focus and uncoupled propagations. In the fourth demonstration, differences were observed between paced and native slow-wave amplitudes (0.24 ± 0.08 vs. 0.38 ± 0.14 mV; P < 0.001), velocities (6.2 ± 2.8 vs. 11.5 ± 4.7 mm/s; P < 0.001), and activated areas (20.6 ± 1.9 vs. 32.8 ± 2.6 cm2; P < 0.001). Entrainment mapping enables an accurate quantification of the effects of gastric pacing on slow-wave activity, offering an improved method to assess whether pacing protocols are likely to achieve physiologically and clinically useful outcomes.
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Inui, Koji, and Ryusuke Kakigi. "Temporal Analysis of the Flow From V1 to the Extrastriate Cortex in Humans." Journal of Neurophysiology 96, no. 2 (August 2006): 775–84. http://dx.doi.org/10.1152/jn.00103.2006.
Повний текст джерелаАнотація:
We previously examined the cortical processing in response to somatosensory, auditory and noxious stimuli, using magnetoencephalography in humans. Here, we performed a similar analysis of the processing in the human visual cortex for comparative purposes. After flash stimuli applied to the right eye, activations were found in eight cortical areas: the left medial occipital area around the calcarine fissure (primary visual cortex, V1), the left dorsomedial area around the parietooccipital sulcus (DM), the ventral (MOv) and dorsal (MOd) parts of the middle occipital area of bilateral hemispheres, the left temporo-occipito-parietal cortex corresponding to human MT/V5 (hMT), and the ventral surface of the medial occipital area (VO) of the bilateral hemispheres. The mean onset latencies of each cortical activity were (in ms): 27.5 (V1), 31.8 (DM), 32.8 (left MOv), 32.2 (right MOv), 33.4 (left MOd), 32.3 (right MOv), 37.8 (hMT), 46.9 (left VO), and 46.4 (right VO). Therefore the cortico-cortical connection time of visual processing at the early stage was 4–6 ms, which is very similar to the time delay between sequential activations in somatosensory and auditory processing. In addition, the activities in V1, MOd, DM, and hMT showed a similar biphasic waveform with a reversal of polarity after 10 ms, which is a common activation profile of the cortical activity for somatosensory, auditory, and pain-evoked responses. These results suggest similar mechanisms of the serial cortico-cortical processing of sensory information among all sensory areas of the cortex.
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Wright, Olivia R. L., Gabriele A. Netzel, and Amy R. Sakzewski. "A randomized, double-blind, placebo-controlled trial of the effect of dried purple carrot on body mass, lipids, blood pressure, body composition, and inflammatory markers in overweight and obese adults: The QUENCH Trial." Canadian Journal of Physiology and Pharmacology 91, no. 6 (June 2013): 480–88. http://dx.doi.org/10.1139/cjpp-2012-0349.
Повний текст джерелаАнотація:
Obesity is a significant health issue worldwide and is associated with chronic, low-grade inflammation predisposing the individual to cardiovascular disease and impaired blood glucose homeostasis. Anthocyanins and phenolic acids from purple carrots are effective at reversing inflammation and metabolic alterations in animal models, potentially through inhibition of inflammatory pathways. The effects of dried purple carrot on body mass, body composition, blood pressure, lipids, inflammatory markers, liver function tests, and appetite were investigated in 16 males (aged 53.1 ± 7.6 years and with a mean BMI of 32.8 ± 4.6 kg/m2) with normal lipid and inflammatory markers. There was no evidence that 118.5 mg/day of anthocyanins and 259.2 mg/day of phenolic acids for 4 weeks resulted in statistically significant changes in body mass, body composition, appetite, dietary intake, low density lipoprotein, total cholesterol, blood pressure, or C-reactive protein in these obese participants at the dose and length of intervention used in this trial. High density lipoprotein cholesterol was lower in the intervention group (p < 0.05). Aspartate amino transferase and alanine amino transferase did not change, indicating that the intervention was safe. More studies are required to establish the bioavailability and pharmacokinetic effects of purple carrot anthocyanins and phenolic acids prior to further trials of efficacy with respect to treating inflammation and metabolic alterations.
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Lee, Yi Lin, Kalyanasundaram Ganesh, Lian Kah Ti, and Shin Yi Ng. "A prospective, observational, longitudinal cohort study of sedation practices in SGH intensive care units." Proceedings of Singapore Healthcare 27, no. 2 (September 26, 2017): 103–9. http://dx.doi.org/10.1177/2010105817731799.
Повний текст джерелаАнотація:
Background: Critically ill patients require sedation for patient comfort and ventilator synchrony. Despite the extensive use of sedation, to date there is no consensus on the best sedation practices. We attempt to investigate our local sedation practices. Method: This was a single-centre prospective, observation cohort study in medical and surgical intensive care unit (ICU) patients who were ventilated and sedated for more than 24 hours. Baseline demographics were obtained and patients followed-up for 28 days or to ICU discharge. Details on sedatives, ventilation duration, vasopressors and renal replacement therapy use, hospital/ICU length of stay, mortality, delirium, and sedation depth were collected and analysed. Results: From March to July 2012, 58 patients were recruited with a mean Acute Physiology and Chronic Health Evaluation II (APACHE II) score of 20.2 ±8.5. Hospital mortality rates were 32.8%. Patients were followed-up for 387 ICU patient-days. In the early period (first 48 h), the most popular sedative used was propofol (74.1%), followed by morphine (29.3%). In the subsequent period (>48 h), most patients were not sedated (47.6%); morphine became the most popular sedation drug (32.5%) followed by propofol (31%). Ketamine, haloperidol and diazepam were not given. In total, 1994 Richmond Agitation and Sedation Score (RASS) assessments were performed over 387 ICU patient-days; 11.1% of RASS assessments were prescribed a sedation target, and 86% of them met the prescribed targets. Delirium was observed in 22.4% of patients. Compared with medical patients, surgical patients were more likely to be prescribed a sedation target (14.2% vs. 7.4%, p<0.01), require lower doses of sedation, have a RASS score of between −2 to 1 (84.8% vs. 72.3%, p<0.01) and have fewer incidences of delirium (4.1% vs. 12.1%, p=0.01). Conclusion: Propofol and morphine were the most commonly prescribed sedatives. Different sedation practices between units may contribute to a reduction in delirium incidence.
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Bogaert, Jan, and Frank E. Rademakers. "Regional nonuniformity of normal adult human left ventricle." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 2 (February 1, 2001): H610—H620. http://dx.doi.org/10.1152/ajpheart.2001.280.2.h610.
Повний текст джерелаАнотація:
Regional nonuniformity is a feature of both diseased and normal left ventricles (LV). With the use of magnetic resonance (MR) myocardial tagging, we performed three-dimensional strain analysis on 87 healthy adults in local cardiac and fiber coordinate systems (radial, circumferential, longitudinal, and fiber strains) to characterize normal nonuniformities and to test the validity of wall thickening as a parameter of regional function. Regional morphology included wall thickness and radii of curvature measurements. With respect to transmural nonuniformity, subendocardial strains exceeded subepicardial strains. Going from base to apex, wall thickness and circumferential radii of curvature decreased, whereas longitudinal radii of curvature increased. All of the strains increased from LV base to apex, resulting in a higher ejection fraction (EF) at the apex than at the base (70.9 ± 0.4 vs. 62.4 ± 0.4%; means ± SE, P < 0.0001). When we looked around the circumference of the ventricle, the anterior part of the LV was the flattest and thinnest and showed the largest wall thickening (46.6 ± 1.2%) but the lowest EF (64.7 ± 0.5%). The posterior LV wall was thicker, more curved, and showed a lower wall thickening (32.8 ± 1.0%) but a higher EF (71.3 ± 0.5%). The regional contribution of the LV wall to the ejection of blood is thus highly variable and is not fully characterized by wall thickening alone. Differences in regional LV architecture and probably local stress are possible explanations for this marked functional nonuniformity.
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Andrási, Terézia B., Anna Blázovics, Gábor Szabó, Christian F. Vahl, and Siegfried Hagl. "Poly(ADP-ribose) polymerase inhibitor PJ-34 reduces mesenteric vascular injury induced by experimental cardiopulmonary bypass with cardiac arrest." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 6 (June 2005): H2972—H2978. http://dx.doi.org/10.1152/ajpheart.01039.2004.
Повний текст джерелаАнотація:
The aim of this study was to investigate effects of poly(ADP-ribose) polymerase (PARP) inhibition on mesenteric vascular function and metabolism in an experimental model of cardiopulmonary bypass (CPB) with cardiac arrest. Twelve anesthetized dogs underwent 90-min hypothermic CPB. After 60 min of cardiac arrest, reperfusion was started for 40 min following application of either saline vehicle (control, n = 6) or a potent PARP inhibitor, PJ-34 (10 mg/kg iv bolus and 0.5 mg·kg−1·min−1 infusion for 20 min, n = 6). PJ-34 led to better recovery of cardiac output (2.2 ± 0.1 vs. 1.8 ± 0.2 l/min in control) and mesenteric blood flow (175 ± 38 vs. 83 ± 4 ml/min, P < 0.05 vs. control) after reperfusion. The impaired vasodilator response of the superior mesenteric artery to acetylcholine, assessed in the control group after CPB (−32.8 ± 3.3 vs. −57.6 ± 6.6% at baseline, P < 0.05), was improved by PJ-34 (−50.3 ± 3.6 vs. −54.3 ± 4.1% at baseline, P < 0.05 vs. control). Although plasma nitrate/nitrite concentrations were not significantly different between groups, mesenteric nitric oxide synthase activity was increased in the PJ-34 group ( P < 0.05). Moreover, the treated group showed a marked attenuation of mesenteric venous plasma myeloperoxidase levels after CPB compared with the control group (75 ± 1 vs. 135 ± 9 ng/ml, P < 0.05). Pharmacological PARP inhibition protects against development of post-CPB mesenteric vascular dysfunction by improving hemodynamics, restoring nitric oxide production, and reducing neutrophil adhesion.
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Lutostansky, Elizabeth M., Gerhard Karner, Gerhard Rappitsch, David N. Ku, and Karl Perktold. "Analysis of Hemodynamic Fluid Phase Mass Transport in a Separated Flow Region." Journal of Biomechanical Engineering 125, no. 2 (April 1, 2003): 189–96. http://dx.doi.org/10.1115/1.1543547.
Повний текст джерелаАнотація:
The mass transfer behavior in the recirculation region downstream of an axisymmetric sudden expansion was examined. The Reynolds number, 500, and Schmidt number, 3200, were selected to model the mass transfer of molecules, such as ADP, in the arterial system. In a first step the transient mass transport applying zero diffusive flux at the wall was analyzed using experiments and two computational codes. The two codes were FLUENT, a commercially available finite volume method, and FTSP, a finite element code developed at Graz University of Technology. The comparison of the transient wall concentration values determined by the three methods was excellent and provides a measure of confidence for computational mass transfer calculations in convection dominated, separated flows. In a second step the effect of the flow separation on the stationary mass transport applying a permeability boundary condition at the water-permeable wall was analyzed using the finite element code FTSP. The results show an increase of luminal ADP surface concentration in the upstream and in the downstream tube of the sudden expansion geometry in the range of six and twelve percent of the bulk flow concentration. The effect of flow separation in the downstream tube on the wall concentration is a decrease of about ten percent of the difference between wall concentration and bulk concentration occurring at nearly fully developed flow at the downstream region at a distance of 66 downstream tube diameters from the expansion. The decrease of ADP flux into the wall is in the range of three percent of the flux at the downstream region.
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Bodenlenz, Manfred, Lukas A. Schaupp, Tatjana Druml, Romana Sommer, Andrea Wutte, Helga C. Schaller, Frank Sinner, Paul Wach, and Thomas R. Pieber. "Measurement of interstitial insulin in human adipose and muscle tissue under moderate hyperinsulinemia by means of direct interstitial access." American Journal of Physiology-Endocrinology and Metabolism 289, no. 2 (August 2005): E296—E300. http://dx.doi.org/10.1152/ajpendo.00431.2004.
Повний текст джерелаАнотація:
Insulin’s action to stimulate glucose utilization is determined by the insulin concentration in interstitial fluid (ISF) of insulin-sensitive tissues. The concentration of interstitial insulin has been measured in human subcutaneous adipose tissue and skeletal muscle, however, never in parallel. The aim of this study was to compare interstitial insulin levels between both tissue beds by simultaneous measurements and to verify and quantify low peripheral ISF insulin fractions as found during moderate hyperinsulinemia. Nine healthy subjects (27.2 ± 0.8 yr) were investigated. A euglycemic-hyperinsulinemic clamp was started with a primed-constant intravenous insulin infusion of 1 mU·kg−1·min−1. For direct access to ISF, macroscopically perforated open-flow microperfusion catheters were inserted in both tissues. During steady-state conditions (9.5 h), interstitial effluents were collected in 30-min fractions using five different insulin concentrations in the inflowing perfusates (“no net flux” protocol). Regression analysis of insulin concentrations in perfusates and effluents yielded the relative recovery and the perfusate insulin concentration, which was in equilibrium with the surrounding tissue. Thus, in subcutaneous adipose tissue and skeletal muscle, the mean ISF-to-serum insulin level was calculated as 21.0% [95% confidence interval (CI) 17.5–24.5] and 26.0% (95% CI 19.1–32.8; P = 0.14), respectively. Recoveries for insulin averaged 51 and 64%, respectively. The data suggest that the concentrations of insulin arising in healthy subjects at the level of ISF per se are comparable between subcutaneous adipose and skeletal muscle tissue. The low interstitial insulin fractions seem to confirm reports of low peripheral insulin levels during moderate insulin clamps.
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Kasińska, Zofia, Piotr Kazimierz Urbański, and Tomasz Tasiemski. "Sports Injuries Among Players of the Polish National Team in Amputee Football in the Annual Training Cycle." Journal of Human Kinetics 81, no. 1 (January 28, 2022): 211–19. http://dx.doi.org/10.2478/hukin-2022-0021.
Повний текст джерелаАнотація:
Abstract The aim of the study was to determine the frequency, type and origin of the occurrence of injuries in amputee football. The studied group comprised all members of the Polish national amputee football team (n = 25). During the 9-month observation period, 13 players incurred 22 injuries. The incidence proportion was 48.0 per 100 athletes (95% Cl, 28.4-67.6) and the incidence rate was 5.73 per 1000 athlete-days (95% Cl, 3.33-8.12). The study showed that 32.8% of the injuries were to the thigh, 13.6% to the ankle, and 9.1% to the knee. The obtained results indicate that amputee football players rather frequently incur play-related injuries, but a single athlete incurs relatively few of them, with the lower limb being most commonly injured.
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Kolla, B., B. J. Coombes, T. I. Morgenthaler, and M. P. Mansukhani. "0173 Spring Forward, Fall Back: Increased Patient Safety-Related Adverse Events Following the Spring Time Change." Sleep 43, Supplement_1 (April 2020): A69. http://dx.doi.org/10.1093/sleep/zsaa056.171.
Повний текст джерелаАнотація:
Abstract Introduction “Spring forward,” the start of daylight savings time (DST) reduces sleep opportunity by an hour. The resulting sleep deprivation in healthcare workers can increase the potential for medical errors. We examined the change in patient safety-related adverse events (AEs) following the time change in both spring and fall. Methods Self-reported AEs that occurred 7 days prior to and following the spring and fall time changes for years 2010–2017 in a large healthcare organization were ascertained. AEs likely resulting from human errors were identified. The change in the number of AEs (all AEs or restricted to those resulting from human error) following the spring and fall time change were modeled using negative binomial mixed models using a random effect to correct for non-independent observations in consecutive. Results Over the 8 year period, there were more AEs (all and human) in the 7 days following the change in time both in spring (All: 2812 V. 2699; Human: 1902 V. 1625) and fall (All: 3207 V. 3007; Human: 2189 V. 2087). However, the only statistically significant increase was for the estimated 18% increase in human errors following time change in spring (95% CI: 6% to 34%; p = 0.004). The 18% AE increase in spring was also significantly greater than the 5% increase in AE in fall (p = 0.018). Conclusion There is a significant increase in human error related AEs following the “spring forward” clock change which can jeopardize patient safety. Based on safety considerations, DST might best be eliminated; alternatively, policy makers and healthcare organizations should evaluate measures to mitigate the increased risk during this period. Support NA
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Brasil, Roxana, Ana Barreto, Leandro Nogueira, Edil Santos, Jefferson Novaes, and Victor Reis. "Comparison of Physiological and Perceptual Responses Between Continuous and Intermittent Cycling." Journal of Human Kinetics 29A, Special-Issue (September 1, 2011): 59–68. http://dx.doi.org/10.2478/v10078-011-0060-7.
Повний текст джерелаАнотація:
Comparison of Physiological and Perceptual Responses Between Continuous and Intermittent CyclingThe present study tested the hypothesis that the exercise protocol (continuous vs. intermittent) would affect the physiological response and the perception of effort during aquatic cycling. Each protocol was divided on four stages. Heart rate, arterial blood pressure, blood lactate concentration, central and peripheral rate of perceived exertion were collected in both protocols in aquatic cycling in 10 women (values are mean ± SD): age=32.8 ± 4.8 years; height=1.62 ± 0.05 cm; body mass=61.60 ± 5.19 kg; estimated body fat=27.13 ± 4.92%. Protocols were compared through two way ANOVA with Scheffé's post-hoc test and the test of Mann- Whitney for rate of perceived exertion with α=0.05. No systematic and consistent differences in heart rate, arterial blood pressure, double product and blood lactate concentration were found between protocols. On the other hand, central rate of perceived exertion was significantly higher at stage four during continuous protocol compared with intermittent protocol (p=0.01), while the peripheral rate of perceived exertion presented higher values at stages three (p=0.02) and four (p=0.00) in the continuous protocol when compared to the results found in intermittent protocol. These findings suggest that although the aquatic cycling induces similar physiologic demands in both protocols, the rate of perceived exertion may vary according to the continuous vs. intermittent nature of the exercise.
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Taraseviciene-Stewart, Laimute, Lajos Gera, Peter Hirth, Norbert F. Voelkel, Rubin M. Tuder, and John M. Stewart. "A bradykinin antagonist and a caspase inhibitor prevent severe pulmonary hypertension in a rat model." Canadian Journal of Physiology and Pharmacology 80, no. 4 (April 1, 2002): 269–74. http://dx.doi.org/10.1139/y02-047.
Повний текст джерелаАнотація:
Chronically hypoxic rats (exposed to 5000 m elevation for 3 weeks) develop pulmonary hypertension (PH) that is reversed upon return to normoxia and is blocked by bradykinin (BK) antagonist B9430 treatment (100 µg/kg s.c. three times per week). Treatment of rats with both the synthetic VEGF receptor-1/2 antagonist 3-[(2,4-dimethylpyrrol- 5-yl)methylidenyl]-indolin-2-one (SU5416) (200 mg/kg, single s.c. injection) and hypoxia (3 weeks) causes irreversible severe PH characterized by marked elevation of pulmonary artery pressure (PAP), right ventricular hypertrophy, and obliteration of pulmonary arteries by proliferating endothelial cells (EC). Between weeks 1 and 2 of treatment, there is increased apoptotic EC death and caspase-3 activity. The combination of hypoxia with VEGFR-1 and -2 blockade appears to cause death of normal lung EC and proliferation of an apoptosis-resistant proliferating EC phenotype. Cotreatment with BK antagonist B9430 and (or) the broad caspase inhibitor Z-Asp-2,6-dichlorobenzoyloxymethylketone (Z-Asp) (2 mg/kg three times per week) prevented development of severe PH and caused significant reduction of PAP: 39.7 ± 4.6 mmHg in Z-Asp + SU5416, 37.1 ± 1.2 mmHg in BK antagonist B9430 + SU5416, 27.2 ± 0.7 mmHg in Z-Asp alone, and 36.6 ± 3.0 mmHg in BK antagonist alone versus 48 ± 1.7 mmHg in SU5416-treated rats and 32.8 ± 1.4 mmHg in vehicle-treated controls. The PAP correlated with the right ventricular mass. Pulmonary arteries of rats treated with Z-Asp and BK antagonist B9430 had a marked reduction of intravascular EC, yet there was still evidence of medial muscular hypertrophy, similar to that observed in chronically hypoxic rats not treated with SU5416. We conclude that EC death induced by VEGFR-2 blockade with SU5416 may trigger an EC selection process that allows for the expansion of apoptosis-resistant EC, possibly driven by mechanisms independent of VEGF and VEGFR-2.Key words: bradykinin antagonist, severe pulmonary hypertension, vascular endothelial growth factor receptors, apoptosis.
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Seewald, M., A. Muench, C. Alio, B. Rosenfield, R. DiTomasso, A. Rostain, J. Ramsay, K. Klingman, and M. L. Perlis. "1111 Do Sleep Disorder Symptom Endorsements Differ Between ADHD Subtypes?" Sleep 43, Supplement_1 (April 2020): A422—A423. http://dx.doi.org/10.1093/sleep/zsaa056.1106.
Повний текст джерелаАнотація:
Abstract Introduction To date, research on differences in sleep complaints between patients with different subtypes of ADHD has been mixed. On balance, the evidence tends towards ADHD-Combined Presentation (ADHD-C) being associated with more severe sleep and sleep-related daytime complaints than ADHD-Primarily Inattentive (ADHD-I). In order to further assess this issue a surveillance study was undertaken in an active ADHD clinic by adding a comprehensive sleep disorders screener (SDS-CL-25) to the clinical intake procedures. These data were used to ascertain whether the two subtypes differ for any of 13 sleep disorders symptoms. Methods Subjects (n = 132; 83 male, 49 female, mean age 32.8, age range 18-79), presenting to the clinic for evaluation for ADHD were given the SDS-CL-25. The SDS-CL-25 is a 25-item instrument developed to screen for multiple sleep disorders at one time (problems are endorsed on a Likert-scale; 0 = never and 4 = more than 5x/week). Endorsements greater than 3x/week were counted as positive for the symptom and less than three days per week was considered negative. Percent per group was compared using Chi Square Analyses. Cumulative morbidity means were also analyzed using t-tests. The subtype, ADHD-I (n=71) and ADHD-C (N=61), was established using EMR records. Results No significant differences between patients with ADHD-I and ADHD-C were detected. Conclusion The lack of finding in the present analysis may reflect a lack of difference or a failure to detect differences based on the small sample sizes or lack of statistical control for likely confounders (age, sex, illness severity or chronicity, SES status, etc.). Analyses are ongoing. Support No support was provided for this abstract.
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Gao, Erhe, Matthieu Boucher, J. Kurt Chuprun, Rui-Hai Zhou, Andrea D. Eckhart, and Walter J. Koch. "Darbepoetin alfa, a long-acting erythropoietin analog, offers novel and delayed cardioprotection for the ischemic heart." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 1 (July 2007): H60—H68. http://dx.doi.org/10.1152/ajpheart.00227.2007.
Повний текст джерелаАнотація:
Recent studies from our lab and others have shown that the hematopoietic cytokine erythropoietin (EPO) can protect the heart from ischemic damage in a red blood cell-independent manner. Here we examined any protective effects of the long-acting EPO analog darbepoetin alfa (DA) in a rat model of ischemia-reperfusion (I/R) injury. Rats were subjected to 30-min ischemia followed by 72-h reperfusion. In a dose-response study, DA (2, 7, 11, and 30 μg/kg) or vehicle was administered as a single bolus at the start of ischemia. To determine the time window of potential cardioprotection, a single high dose of DA (30 μg/kg) was given at either the initiation or the end of ischemia or at 1 or 24 h after reperfusion. After 3 days, cardiac function and infarct size were assessed. Acute myocyte apoptosis was quantified by TUNEL staining on myocardial sections and by caspase-3 activity assays. DA significantly reduced infarct size from 32.8 ± 3.5% (vehicle) to 11.0 ± 3.3% in a dose-dependent manner, while there was no difference in ischemic area between groups. Treatment with DA as late as 24 h after the beginning of reperfusion still demonstrated a significant reduction in infarct size (17.0 ± 1.6%). Consistent with infarction data, DA improved in vivo cardiac reserve compared with vehicle. Finally, DA significantly decreased myocyte apoptosis and caspase-3 activity after I/R. These data indicate that DA protects the heart against I/R injury and improves cardiac function, apparently through a reduction of myocyte apoptosis. Of clinical importance pointing toward a relevant therapeutic utility, we report that even if given 24 h after I/R injury, DA can significantly protect the myocardium.
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Carlsson, Ola, and Bengt Rippe. "Peritoneal lymphatic absorption and solute exchange during zymosan-induced peritonitis in the rat." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 3 (September 1, 1999): H1107—H1112. http://dx.doi.org/10.1152/ajpheart.1999.277.3.h1107.
Повний текст джерелаАнотація:
Lymph flow is elevated in most inflammatory conditions. However, a few previous studies have indicated that peritoneal lymph flow may actually fall during acute peritonitis. This study was performed to explore this issue further and to study the pathophysiology of peritoneal exchange during peritonitis. Therefore, we wanted to assess the total peritoneal clearance (Cl) and the clearance from peritoneum to plasma (Cl → P) of125I-labeled albumin (125I-albumin) as well as plasma-to-dialysate clearance (Cl → D) of Evans blue-labeled albumin together with peritoneal ultrafiltration (UF) profiles and mass transfer area coefficients of51Cr-EDTA and glucose in rats after acute peritonitis induced by zymosan. Zymosan incubation of the peritoneal cavity (120 mg) for 4 h generally led to a 4- to 10-fold increase in peritoneal fluid white blood cell count, indicating that acute peritonitis had been induced. Then 16 ml of 3.86% Dianeal and125I-albumin were instilled intraperitoneally, whereas Evans blue-labeled albumin and51Cr-EDTA were given as infusions intravenously. Compared with control, mass transfer area coefficients for glucose and51Cr-EDTA increased markedly from 0.43 ± 0.06 and 0.25 ± 0.04 to 0.91 ± 0.06 and 0.59 ± 0.05 (SE) ml/min, respectively, during peritonitis, whereas Cl and Cl → D increased from 32.8 ± 5.6 and 8.6 ± 1.6 to 74.5 ± 7.3 and 12.9 ± 1.0 μl/min, respectively. The UF profile in peritonitis indicated type I loss of UF (resulting from the increases in permeability-surface area product for glucose). However, the Cl → P declined to 5.9 ± 1.0 μl/min from 7.9 ± 0.8 μl/min ( P < 0.05) in control. In conclusion, despite marked effects on peritoneal solute transport and on UF, conceivably resulting from vasodilatation and increases in capillary permeability, zymosan-induced peritonitis did not cause any acute increases in direct peritoneal lymphatic absorption.
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Seol, Geun Hee, Seung Cheol Ahn, Ji Aee Kim, Bernd Nilius, and Suk Hyo Suh. "Inhibition of endothelium-dependent vasorelaxation by extracellular K+: a novel controlling signal for vascular contractility." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 1 (January 2004): H329—H339. http://dx.doi.org/10.1152/ajpheart.00503.2003.
Повний текст джерелаАнотація:
The effects of extracellular K+ on endothelium-dependent relaxation (EDR) and on intracellular Ca2+ concentration ([Ca2+]i) were examined in mouse aorta, mouse aorta endothelial cells (MAEC), and human umbilical vein endothelial cells (HUVEC). In mouse aortic rings precontracted with prostaglandin F2α or norepinephrine, an increase in extracellular K+ concentration ([K+]o) from 6 to 12 mM inhibited EDR concentration dependently. In endothelial cells, an increase in [K+]o inhibited the agonist-induced [Ca2+]i increase concentration dependently. Similar to K+, Cs+ also inhibited EDR and the increase in [Ca2+]i concentration dependently. In current-clamped HUVEC, increasing [K+]o from 6 to 12 mM depolarized membrane potential from –32.8 ± 2.7 to –8.6 ± 4.9 mV ( n = 8). In voltage-clamped HUVEC, depolarizing the holding potential from –50 to –25 mV decreased [Ca2+]i significantly from 0.95 ± 0.03 to 0.88 ± 0.03 μM ( n = 11, P < 0.01) and further decreased [Ca2+]i to 0.47 ± 0.04 μM by depolarizing the holding potential from –25 to 0 mV ( n = 11, P < 0.001). Tetraethylammonium (1 mM) inhibited EDR and the ATP-induced [Ca2+]i increase in voltage-clamped MAEC. The intermediate-conductance Ca2+-activated K+ channel openers 1-ethyl-2-benzimidazolinone, chlorozoxazone, and zoxazolamine reversed the K+-induced inhibition of EDR and increase in [Ca2+]i. The K+-induced inhibition of EDR and increase in [Ca2+]i was abolished by the Na+-K+ pump inhibitor ouabain (10 μM). These results indicate that an increase of [K+]o in the physiological range (6–12 mM) inhibits [Ca2+]i increase in endothelial cells and diminishes EDR by depolarizing the membrane potential, decreasing K+ efflux, and activating the Na+-K+ pump, thereby modulating the release of endothelium-derived vasoactive factors from endothelial cells and vasomotor tone.
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Solomon, Thomas P. J., Jacob M. Haus, Christine M. Marchetti, William C. Stanley, and John P. Kirwan. "Effects of exercise training and diet on lipid kinetics during free fatty acid-induced insulin resistance in older obese humans with impaired glucose tolerance." American Journal of Physiology-Endocrinology and Metabolism 297, no. 2 (August 2009): E552—E559. http://dx.doi.org/10.1152/ajpendo.00220.2009.
Повний текст джерелаАнотація:
Elevated free fatty acids (FFA) are implicated with insulin resistance at the cellular level. However, the contribution of whole body lipid kinetics to FFA-induced insulin resistance is not well understood, and the effect of exercise and diet on this metabolic defect is not known. We investigated the effect of 12 wk of exercise training with and without caloric restriction on FFA turnover and oxidation (FFAox) during acute FFA-induced insulin resistance. Sixteen obese subjects with impaired glucose tolerance were randomized to either a hypocaloric ( n = 8; −598 ± 125 kcal/day, 66 ± 1 yr, 32.8 ± 1.8 kg/m2) or a eucaloric ( n = 8; 67 ± 2 yr, 35.3 ± 2.1 kg/m2) diet and aerobic exercise (1 h/day at 65% of maximal oxygen uptake) regimen. Lipid kinetics ([1-14C]palmitate) were assessed throughout a 7-h, 40 mU·m−2·min−1 hyperinsulinemic euglycemic clamp, during which insulin resistance was induced in the last 5 h by a sustained elevation in plasma FFA (intralipid/heparin infusion). Despite greater weight loss in the hypocaloric group (−7.7 ± 0.5 vs. −3.3 ± 0.7%, P < 0.001), FFA-induced peripheral insulin resistance was improved equally in both groups. However, circulating FFA concentrations (2,123 ± 261 vs. 1,764 ± 194 μmol/l, P < 0.05) and FFA turnover (3.20 ± 0.58 vs. 2.19 ± 0.58 μmol·kg FFM−1·min−1, P < 0.01) during hyperlipemia were suppressed only in the hypocaloric group. In contrast, whole body FFAox was improved in both groups at rest and during hyperlipemia. These changes were driven by increases in intracellular lipid-derived FFAox (12.3 ± 7.7 and 14.7 ± 7.8%, P < 0.05). We conclude that the exercise-induced improvement in FFA-induced insulin resistance is independent of the magnitude of weight loss and FFA turnover, yet it is linked to increased intracellular FFA utilization.
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Creely, S. J., P. G. McTernan, C. M. Kusminski, ff M. Fisher, N. F. Da Silva, M. Khanolkar, M. Evans, A. L. Harte, and S. Kumar. "Lipopolysaccharide activates an innate immune system response in human adipose tissue in obesity and type 2 diabetes." American Journal of Physiology-Endocrinology and Metabolism 292, no. 3 (March 2007): E740—E747. http://dx.doi.org/10.1152/ajpendo.00302.2006.
Повний текст джерелаАнотація:
Type 2 diabetes (T2DM) is associated with chronic low-grade inflammation. Adipose tissue (AT) may represent an important site of inflammation. 3T3-L1 studies have demonstrated that lipopolysaccharide (LPS) activates toll-like receptors (TLRs) to cause inflammation. For this study, we 1) examined activation of TLRs and adipocytokines by LPS in human abdominal subcutaneous (AbdSc) adipocytes, 2) examined blockade of NF-κB in human AbdSc adipocytes, 3) examined the innate immune pathway in AbdSc AT from lean, obese, and T2DM subjects, and 4) examined the association of circulating LPS in T2DM subjects. The findings showed that LPS increased TLR-2 protein expression twofold ( P < 0.05). Treatment of AbdSc adipocytes with LPS caused a significant increase in TNF-α and IL-6 secretion (IL-6, Control: 2.7 ± 0.5 vs. LPS: 4.8 ± 0.3 ng/ml; P < 0.001; TNF-α, Control: 1.0 ± 0.83 vs. LPS: 32.8 ± 6.23 pg/ml; P < 0.001). NF-κB inhibitor reduced IL-6 in AbdSc adipocytes (Control: 2.7 ± 0.5 vs. NF-κB inhibitor: 2.1 ± 0.4 ng/ml; P < 0.001). AbdSc AT protein expression for TLR-2, MyD88, TRAF6, and NF-κB was increased in T2DM patients ( P < 0.05), and TLR-2, TRAF-6, and NF-κB were increased in LPS-treated adipocytes ( P < 0.05). Circulating LPS was 76% higher in T2DM subjects compared with matched controls. LPS correlated with insulin in controls ( r = 0.678, P < 0.0001). Rosiglitazone (RSG) significantly reduced both fasting serum insulin levels (reduced by 51%, P = 0.0395) and serum LPS (reduced by 35%, P = 0.0139) in a subgroup of previously untreated T2DM patients. In summary, our results suggest that T2DM is associated with increased endotoxemia, with AT able to initiate an innate immune response. Thus, increased adiposity may increase proinflammatory cytokines and therefore contribute to the pathogenic risk of T2DM.
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Guzman, Johann Paulo Suico, Leandro L. Resurreccion III, Marcus Lester R. Suntay, and Renato G. Bernaldez. "Comparison between hepaticojejunostomy and hepaticoduodenostomy after excision of choledochal cyst in children: a cohort study." World Journal of Pediatric Surgery 2, no. 2 (June 2019): e000029. http://dx.doi.org/10.1136/wjps-2018-000029.
Повний текст джерелаАнотація:
ObjectiveHepaticojejunostomy (HJ) and hepaticoduodenostomy (HD) are commonly used biliary reconstruction techniques after choledochal cyst excision. HD has been suggested to be a more physiologic alternative during reconstruction. The objective of this study is to compare operative time, hospital stay, morbidity (leak, cholangitis, ileus, and obstruction), and mortality between HJ and HD after cyst excision.MethodsThis is a 14-year retrospective cohort study of pediatric patients (≤18 years old) who underwent choledochal cyst excision and subsequent biliary reconstruction at the Philippine Children’s Medical Center. Data were taken from inpatient charts, operative technique, OPD logbook, readmission, and OPD charts.ResultsThere were 122 patients: 56% HD and 44% HJ. Majority were female (72%), with 1:2.6 male to female ratio. The average age was 36.1 months, with a mean follow-up of 32.8 months (range 6 months–14 years). The most common cyst was type I (87%). Operative time was longer for HJ compared with HD (321.3 vs 203.6 min; p=0.000). Hospital stay was longer with HJ compared with HD (7.7 vs 6.8 days; p=0.002). Mortality rate was low at 1.6% while morbidity was at 13.9% in both groups. Although morbidity was higher among those who underwent HD, there was no significant difference between the two procedures. Anastomotic leak (4%) and cholangitis (7.4%) were observed in HD, and ileus (7.4%) was observed in the HJ group.ConclusionsIn our series, HD provided less operative time and hospital stay than with HJ. We did not observe bile gastritis after HD as compared with others. It is suggested that longer follow-up is needed to confirm such findings.