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1
Armstrong, C., KW Burak, and PL Beck. "Benzocaine-Induced Methemoglobinemia: A Condition of which all Endoscopists Should Be Aware." Canadian Journal of Gastroenterology 18, no. 10 (2004): 625–29. http://dx.doi.org/10.1155/2004/620203.
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Methemoglobinemia is a rare complication that can occur with the use of benzocaine-containing compounds. Two cases of methemoglobinemia are reported, and the pathophysiology and treatment of methemoglobinemia are reviewed. Both patients received topical 20% benzocaine spray before endoscopy. Immediately following the procedure, there was a reduction in O2saturation assessed by pulse oximetry that was refractory to O2therapy. Dramatic peripheral and central cyanosis developed. O2saturation measured by pulse oximetry ranged from 83% to 87% on O2by nasal prongs and 100% O2by a nonrebreathing mask. Both patients were mildly confused and one patient complained of a significant headache. The diagnosis of methemoglobinemia was considered and arterial blood gas sampling was performed. In both patients, the arterial blood had a chocolate brown colour. A methemoglobin level of 48% and 18% was noted in patient 1 and patient 2, respectively. Both patients were treated with methylene blue, resulting in a significant improvement with gradual normalization of their O2saturation within 10 min to 30 min. The use of benzocaine spray may not markedly alter the patient's perception of endoscopy and thus, the routine use of these agents should be questioned. If such agents are used, the physician must be aware of this association to prevent a delay in the diagnosis and management of this rare, but potentially lethal, condition.
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SEO, YOOJIN, KAZUYA MATSUMOTO, YOUNG MAN PARK, MOTOHIKO MOHRI, SHIGEAKI MATSUOKA, and KWANG PAK PARK. "Changes in sleep patterns during He-O2saturation dives." Psychiatry and Clinical Neurosciences 52, no. 2 (1998): 141–42. http://dx.doi.org/10.1111/j.1440-1819.1998.tb00995.x.
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Bloos, F., and K. Reinhart. "The value of central venous O2saturation for assessment of tissue oxygenation." DMW - Deutsche Medizinische Wochenschrift 129, no. 48 (2004): 2601–4. http://dx.doi.org/10.1055/s-2004-836082.
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Moszura, Tomasz, Pawel Dryzek, Sebastian Goreczny, et al. "A 10-year single-centre experience in percutaneous interventions for multi-stage treatment of hypoplastic left heart syndrome." Cardiology in the Young 24, no. 1 (2013): 54–63. http://dx.doi.org/10.1017/s104795111200220x.
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AbstractObjectivesThe purpose of this paper is to report our 10 years of experience of interventional treatment of patients with hypoplastic left heart syndrome and to focus on the frequency, type, and results of percutaneous interventions during all the stages of palliation, considering the different techniques, devices, and complications.BackgroundConstant progress in surgical treatment of congenital heart defects in the last decade has significantly improved the prognosis for children with hypoplastic left heart syndrome. However, morbidity and mortality remain relatively high. Modern interventional procedures complement or occasionally replace surgical treatment.MethodsBetween January, 2001 and December, 2010, 161 percutaneous interventions were performed in 88 patients with hypoplastic left heart syndrome. Patients were divided into four groups: (a) before the first surgical treatment including hybrid approach, (b) after first-stage Norwood operation, (c) after second-stage bidirectional Glenn operation, and (d) after third-stage Fontan operation.ResultsPercutaneous interventions resulted in statistically significant changes in pulmonary artery pressures, vessel diameters, and O2saturation. Complications occurred in 4.3% of interventions and were related mainly to stent implantation in stenosed pulmonary arteries.ConclusionsPercutaneous interventions may result in haemodynamic stability and reduction in the number of operations. They may result in significant changes in pulmonary artery pressures, vessel diameters, O2saturation, with a low rate of complications, which are mainly related to stent implantation in the pulmonary arteries.
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Crocker, George H., Balazs Toth, and James H. Jones. "Combined effects of inspired oxygen, carbon dioxide, and carbon monoxide on oxygen transport and aerobic capacity." Journal of Applied Physiology 115, no. 5 (2013): 643–52. http://dx.doi.org/10.1152/japplphysiol.01407.2012.
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We hypothesized that breathing hypoxic, hypercapnic, and CO-containing gases together reduces maximal aerobic capacity (V̇o2max) as the sum of each gas' individual effect on V̇o2max. To test this hypothesis, goats breathed combinations of inspired O2fraction (FiO2) of 0.06–0.21 and inspired CO2fraction of 0.00 or 0.05, with and without inspired CO that elevated carboxyhemoglobin fraction (FHbCO) to 0.02–0.45, while running on a treadmill at speeds eliciting V̇o2max. Individually, hypoxia and elevated FHbCOdecreased fractional V̇o2max(FV̇o2max, fraction of a goat's V̇o2maxbreathing air) in linear, dose-dependent manners; hypercapnia did not change V̇o2max. Concomitant hypoxia and elevated FHbCOdecreased V̇o2maxless than the individual gas effects summed, indicating their combined effects on V̇o2maxare attenuated, fitting the following regression: FV̇o2max= 4.24 FiO2+ 0.519 FHbCO− 8.22 (FiO2× FHbCO) + 0.117, ( R2= 0.965, P < 0.001). The FV̇o2maxcorrelated highly with total cardiopulmonary O2delivery, not peripheral diffusing capacity, and with arterial O2concentration (CaO2), not cardiac output. Hypoxia and elevated FHbCOdecreased CaO2by different mechanisms: hypoxia decreased arterial O2saturation (SaO2), whereas elevated FHbCOdecreased O2capacitance {concentration of hemoglobin (Hb) available to bind O2([Hbavail])}. When breathing hypoxic gas (FiO20.12), CaO2did not change with increasing FHbCOup to 0.30 because higher SaO2of Hbavailoffset decreased [Hbavail] due to the following: 1) hyperventilation with hypoxia and/or elevated FHbCO; 2) increased Hb affinity for O2due to both Bohr and direct carboxyhemoglobin effects; and 3) the sigmoid relationship between O2saturation and partial pressure elevating SaO2more with hypoxia than normoxia.
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Hall, David M., Kirk R. Baumgardner, Terry D. Oberley, and Carl V. Gisolfi. "Splanchnic tissues undergo hypoxic stress during whole body hyperthermia." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 5 (1999): G1195—G1203. http://dx.doi.org/10.1152/ajpgi.1999.276.5.g1195.
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Exposure of conscious animals to environmental heat stress increases portal venous radical content. The nature of the observed heat stress-inducible radical molecules suggests that hyperthermia produces cellular hypoxic stress in liver and intestine. To investigate this hypothesis, conscious rats bearing in-dwelling portal venous and femoral artery catheters were exposed to normothermic or hyperthermic conditions. Blood gas levels were monitored during heat stress and for 24 h following heat exposure. Hyperthermia significantly increased arterial O2saturation, splanchnic arterial-venous O2difference, and venous[Formula: see text], while decreasing venous O2saturation and venous pH. One hour after heat exposure, liver glycogen levels were decreased ∼20%. Two hours after heat exposure, the splanchnic arterial-venous O2difference remained elevated in heat-stressed animals despite normal Tc. A second group of rats was exposed to similar conditions while receiving intra-arterial injections of the hypoxic cell marker [3H]misonidazole. Liver and intestine were biopsied, and [3H]misonidazole content was quantified. Heat stress increased tissue [3H]misonidazole retention 80% in the liver and 29% in the small intestine. Cellular [3H]misonidazole levels were significantly elevated in intestinal epithelial cells and liver zone 2 and 3 hepatocytes and Kupffer cells. This effect was most prominent in the proximal small intestine and small liver lobi. These data provide evidence that hyperthermia produces cellular hypoxia and metabolic stress in splanchnic tissues and suggest that cellular metabolic stress may contribute to radical generation during heat stress.
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Morse, John WI, Sharyle A. Fowler, and Amy L. Morse. "Endoscopist-Administered Propofol: A Retrospective Safety Study." Canadian Journal of Gastroenterology 22, no. 7 (2008): 617–20. http://dx.doi.org/10.1155/2008/265465.
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BACKGROUND: Propofol is an anesthetic agent that is commonly used for conscious sedation. Propofol has advantages as a sedative agent for endoscopic procedures including rapid onset, short half-life and rapid recovery time. However, concerns exist regarding the potential for respiratory depression, hypotension, perforation due to deep sedation and the need for monitoring by an anesthetist. Propofol has been used under endoscopist supervision at the Stanton Territorial Hospital in Yellowknife, Northwest Territories since 1996 (approximately 7000 cases).METHODS: A retrospective chart review of endoscopic procedures conducted at the Stanton Territorial Hospital between January 1996 and May 2007 was performed. A random sample of 680 procedures was reviewed from a total of 6396 procedures.RESULTS: The mean (± SD) baseline systolic blood pressure (SBP) was 122.8±17.0 mmHg. The mean lowest SBP was 101.7±14.5 mmHg. The mean absolute drop in SBP was 21.1±16.7 mmHg, with a mean per cent drop of 16.3%±11.7%. Eighty-eight patients (12.9%) developed transient hypotension (SBP lower than 90 mmHg). All patients regained normal blood pressure spontaneously on repeated measurement. No patients required intravenous fluid resuscitation. The mean O2saturation was 96.4%±2.1%. One patient (0.1%) transiently desaturated (O2saturation 89%), but recovered spontaneously on repeat measurement with no intervention. No procedures were aborted for patient safety. There were no major complications, including perforation or death. There was one mucosal tear during nontherapeutic colonoscopy (0.1%).CONCLUSIONS: Propofol can be safely administered in a community hospital setting under endoscopist supervision, with no additional support or monitoring.
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Kawakami, Michiro, Kazuo Makimoto, Osamu Noi, and Hiroaki Takahashi. "Feasibility of Pulse Oxymetry to Measure Arterial O2Saturation in Studies on Cochlear Blood Circulation." Acta Oto-Laryngologica 111, no. 5 (1991): 908–16. http://dx.doi.org/10.3109/00016489109138429.
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Milingos, D., D. Doumplis, K. Sieunarine, P. Savage, A. D. Lawson, and J. R. Smith. "Uterine arteriovenous malformation: fertility-sparing surgery using unilateral ligation of uterine artery and ovarian ligament." International Journal of Gynecologic Cancer 17, no. 3 (2007): 735–37. http://dx.doi.org/10.1136/ijgc-00009577-200705000-00028.
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Arteriovenous malformations (AVM) are rarely found in the uterus and are usually acquired. The method of treatment is determined by symptoms, desire for future fertility, extent, and location of the malformation. Selective ligation of the vessels supplying the malformation is an effective treatment option when conservative methods have failed and uterine preservation is of primary concern. Measurement of uterine O2saturation and perfusion index has been shown to be effective in the intraoperative assessment of uterine viability, pre- and postligation of pelvic vasculature. We present the case of a 32-year-old woman with a postmolar uterine AVM treated surgically with unilateral uterine artery and ovarian ligament ligation.
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Dufu, Kobina, Ozlem Yalcin, Eilleen S. Y. Ao-ieong, et al. "GBT1118, a potent allosteric modifier of hemoglobin O2affinity, increases tolerance to severe hypoxia in mice." American Journal of Physiology-Heart and Circulatory Physiology 313, no. 2 (2017): H381—H391. http://dx.doi.org/10.1152/ajpheart.00772.2016.
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Adaptation to hypoxia requires compensatory mechanisms that affect O2transport and utilization. Decreased hemoglobin (Hb) O2affinity is considered part of the physiological adaptive process to chronic hypoxia. However, this study explores the hypothesis that increased Hb O2affinity can complement acute physiological responses to hypoxia by increasing O2uptake and delivery compared with normal Hb O2affinity during acute severe hypoxia. To test this hypothesis, Hb O2affinity in mice was increased by oral administration of 2-hydroxy-6-{[(2 S)-1-(pyridine-3-carbonyl)piperidin-2yl] methoxy}benzaldehyde (GBT1118; 70 or 140 mg/kg). Systemic and microcirculatory hemodynamics and oxygenation parameters were studied during hypoxia in awake-instrumented mice. GBT1118 increased Hb O2affinity and decreased the Po2at which 50% of Hb is saturated with O2(P50) from 43 ± 1.1 to 18.3 ± 0.9 mmHg (70 mg/kg) and 7.7 ± 0.2 mmHg (140 mg/kg). In a dose-dependent fashion, GBT1118 increased arterial O2saturation by 16% (70 mg/kg) and 40% (140 mg/kg) relative to the control group during 5% O2hypoxia. In addition, a GBT1118-induced increase in Hb O2affinity reduced hypoxia-induced hypotension compared with the control group. Moreover, microvascular blood flow was higher during hypoxia in GBT1118-treated groups than the control group. The increased O2saturation and improved blood flow in GBT1118-treated groups preserved higher interstitial tissue Po2than in the control group during 5% O2hypoxia. In conclusion, increased Hb O2affinity enhanced physiological tolerance to hypoxia, as evidenced by improved hemodynamics and tissue oxygenation. Therefore, pharmacologically induced increases in Hb O2affinity become a potential therapeutic approach to improve tissue oxygenation in pulmonary diseases characterized by severe hypoxemia.NEW & NOTEWORTHY This study establishes that pharmacological modification of hemoglobin O2affinity can be a promising and novel therapeutic strategy for the treatment of hypoxic hypoxia and paves the way for the clinical development of molecules that prevent hypoxemia.
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Rampil°, I. J., L. Litt°, and A. Mayevsky. "CORRELATED MULTIPLE-WAVELENGTH MONITORING OF LOCALIZED CEREBRO-CORTICAL NADH AND BRAIN MICRO-VESSEL HEMOGLOBIN O2SATURATION." Anesthesiology 75, no. 3 (1991): A446. http://dx.doi.org/10.1097/00000542-199109001-00446.
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Iwase, N., Y. Kikuchi, W. Hida, et al. "Effects of Repetitive Airway Obstruction on O2Saturation and Systemic and Pulmonary Arterial Pressure in Anesthetized Dogs." American Review of Respiratory Disease 146, no. 6 (1992): 1402–10. http://dx.doi.org/10.1164/ajrccm/146.6.1402.
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Zeraati, Mohammad Reza, and Taraneh Naghibi. "Acute Pulmonary Edema Following Administration of Magnesium Sulfate in a Pregnant Patient." Journal of Advances in Medical and Biomedical Research 27, no. 124 (2019): 43–46. https://doi.org/10.30699/jambs.27.124.43.
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Acute pulmonary edema affects 0.08% to 1.5% of women during pregnancy and during the postpartum period, and preeclampsia/eclampsia is a major obstetric cause of acute pulmonary edema. We present a case of a 23-year-old nulliparous woman who was referred totertiary medical center for preterm labor and dyspnea (Mousavi Hospital). The patient complained of having suddenly developed respiratory distress and a decrease in O2saturation following the administration of magnesium sulfate. A chest radiograph taken at bedside showed widespread interstitial shadowing consistent with pulmonary edema. The patient was given prompt treatment, and she achieved full recovery. Pharmacological agents are one of the defendants used for lung edema during pregnancy. It is important to pay attention to lung edema due to tocolytic administration. <strong>Keywords: </strong>Magnesium sulfate, Pulmonary edema, Tocolytic, Pregnancy
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Pajk, Werner, Birgit Schwarz, Hans Knotzer, et al. "Jejunal tissue oxygenation and microvascular flow motion during hemorrhage and resuscitation." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 6 (2002): H2511—H2517. http://dx.doi.org/10.1152/ajpheart.00222.2002.
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The relationship between flow motion and tissue oxygenation was investigated during hemorrhage/retransfusion with and without dopamine in 14 pigs. During 45% bleed, jejunal microvascular hemoglobin O2saturation (HBjO2) and mucosal tissue Po2(Po2muc) were recorded in seven control and seven dopamine-treated animals. Mean arterial pressure and systemic O2delivery decreased during hemorrhage and returned to baseline after retransfusion. Hemorrhage decreased Po2mucfrom 33 ± 2.8 to 13 ± 1.6 mmHg and HBjO2from 53 ± 4.9% to 32 ± 3.9%, respectively, in control animals. During reperfusion, Po2mucand HBjO2remained low. Dopamine increased Po2mucfrom 28 ± 4.3 to 45 ± 4.6 mmHg and HBjO2from 54 ± 5.7% to 69 ± 1.5% and attenuated the decrease in Po2mucand HBjO2during hemorrhage. After retransfusion, dopamine restored Po2mucand HBjO2to baseline. Control animals developed rhythmic HBjO2oscillations with increasing amplitude (frequency, 4.5 to 7.6 cycles/min) and showed an inverse relationship between Po2mucand HBjO2oscillation amplitude. Dopamine prevented regular flow motion. The association between decreased Po2mucand increased oscillations in HBjO2after normalization of systemic hemodynamics and O2transport in control animals suggests a cause-and-effect relationship between low tissue Po2and flow motion activity within the jejunal microcirculation.
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Crisostomo, Isabel, Adel Zayyad, David W. Carley, et al. "Chemo- and baroresponses differ in African-Americans and Caucasians in sleep." Journal of Applied Physiology 85, no. 4 (1998): 1413–20. http://dx.doi.org/10.1152/jappl.1998.85.4.1413.
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To determine sleep effects on baro- and ventilatory responses to transient chemo- and barostimulation in African-Americans and Caucasians, 26 nonobese normotensive young subjects (13 African-Americans and 13 Caucasians) were studied awake and in non-rapid-eye movement (NREM) and rapid-eye-movement sleep during induced transient hypoxemia (N2), hypertension (phenylephrine, PE), and concomitant hypoxemia and hypertension (N2 + PE). Arterial blood pressure was recorded by plethysmographic volume clamp, minute ventilation by pneumotachograph, and arterial O2saturation by pulse oximeter. For all subjects, chronotropic baroresponse (Δpulse interval/Δsystolic blood pressure, where Δ is change) increased with NREM sleep ( P = 0.007). Baroresponse slope was greater in Caucasians than in African-Americans (ANOVA, P = 0.02). Hypoxemic ventilatory response (Δminute ventilation/Δarterial O2 saturation) was greater in African-Americans than in Caucasians in NREM sleep ( P = 0.01), as was hypoxemic attenuation of baroresponse (N2 + PE, P = 0.03). These data suggest sleep-related differences in arterial chemo- and baroreceptor responses in normal young African-Americans and Caucasians, which may have implications concerning development of systemic hypertension.
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Moss, Timothy J., and Richard Harding. "Ventilatory and arousal responses of sleeping lambs to respiratory challenges: effect of prenatal maternal anemia." Journal of Applied Physiology 88, no. 2 (2000): 641–48. http://dx.doi.org/10.1152/jappl.2000.88.2.641.
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We have examined the effects of exposure to chronic maternal anemia, throughout the final one-third of gestation, on postnatal ventilatory and arousal responses to hypoxia, hypercapnia, and combined hypoxia-hypercapnia in sleeping lambs. While resting quietly awake, lambs from anemic ewes had higher arterial [Formula: see text] levels than control animals during the first 2–3 postnatal wk, but pH, arterial [Formula: see text], and arterial O2 saturation were not different. During active and quiet sleep lambs from anemic ewes had higher end-tidal CO2levels than control animals when breathing room air and at the time of spontaneous arousal or when aroused by progressive hypercapnia or by combined hypoxia-hypercapnia. Ventilation and arterial O2saturation during uninterrupted sleep and ventilatory responsiveness to hypoxia (inspiratory O2 fraction, 10%), progressive hypercapnia, and combined hypoxia/hypercapnia were not significantly affected by exposure to maternal anemia. Our findings show that maternal anemia results in elevated[Formula: see text] levels in the offspring. This effect may be due, at least in part, to altered pulmonary function.
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Muzyamba, M. C., P. F. Speake, and J. S. Gibson. "Oxidants and regulation of K+-Cl−cotransport in equine red blood cells." American Journal of Physiology-Cell Physiology 279, no. 4 (2000): C981—C989. http://dx.doi.org/10.1152/ajpcell.2000.279.4.c981.
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The effect of oxidants on K+-Cl−cotransport (KCC) was investigated in equine red blood cells. Carbon monoxide mimicked O2. The substituted benzaldehyde, 12C79 (5 mM), markedly increased O2affinity. In N2, however, O2saturation was low (<10%) but KCC remained active. Nitrite (NO2−) oxidized heme to methemoglobin (metHb). High concentrations of NO2−(1 and 5 mM vs. 0.5 mM) increased KCC activity above control levels; it became O2independent but remained sensitive to other stimuli. 1-Chloro-2,4-dinitrobenzene (1–3 mM) depleted reduced glutathione (GSH). Prolonged exposure (60–120 min, 1 mM) or high concentrations (3 mM) stimulated an O2-independent KCC activity; short exposures and low concentrations (30 min, 0.5 or 1 mM) did not. The effect of these manipulations was correlated with changes in GSH and metHb concentrations. An oxy conformation of Hb was necessary for KCC activation. An increase in its activity over the level found in oxygenated control cells required both accumulation of metHb and depletion of GSH. Findings are relevant to understanding the physiology and pathology of regulation of KCC.
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Soomro, Niaz Hussain Soomro, Hamid Mehmood, M. Aleemud Din, Aneeqa Ahsan Zafar, and Sadaf Siddiqui. "THORACIC EPIDURAL ANALGESIA." Professional Medical Journal 23, no. 08 (2016): 975–79. http://dx.doi.org/10.29309/tpmj/2016.23.08.1672.
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Objectives: The aim of this study is to determine whether thoracic epiduralanalgesia with bupivacaine is better than intravenous narcotic analgesia for pain relief inthoracotomy patients. Study design: Prospective randomized study. Setting: Department ofThoracic Surgery, Ojha Institute of Chest Diseases and Dow University of Health Sciences.Period: May 2014- Nov 2015. Methods: 144 patients were allocated randomly into 2 Groups.Group A received thoracic epidural analgesia with bupivacaine and Group B received intravenousnarcotic analgesia with tramadol. Pain was monitored in both groups using the VAS pain scaleevery hour for the first 6 hours and then at 20, 24, 30, and 48 hours postoperatively. Results: Itwas observed that Group A patients experienced less pain at rest, coughing and on movementsas compared to patients in Group B throughout the monitoring from first hour to 48 hourspostoperatively. There was no significant difference between the groups in respiratory rate, O2saturation, adverse effects and performance status on day one and day two postoperatively.The mean hospital stay after operation was 7 days in both groups. Conclusions: Optimal painrelief after thoracotomy improves patient recovery and satisfaction. We determined that thoracicepidural analgesia with bupivacaine is better than intravenous narcotic analgesia for pain reliefin thoracotomy patients.
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Srinivasan, Ganesh, Eugene N. Bruce, Pamela K. Houtz, and Margaret C. Bruce. "Dexamethasone-induced changes in lung function are not prevented by concomitant treatment with retinoic acid." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 2 (2002): L275—L287. http://dx.doi.org/10.1152/ajplung.00423.2001.
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Alveolarization is impaired in rats treated with dexamethasone (Dex) on postnatal days 4–13, but concomitant treatment with all- trans retinoic acid (RA) increases alveolar number. To determine whether morphological changes induced by Dex and/or RA predict changes in lung function at 1 mo, we assessed resting breathing parameters, dynamic compliance, ventilation required to maintain O2 saturation at ≥90%, and pressure-volume curves of air-filled lungs. During resting breathing, mean tidal volume per gram was greater in Dex + RA-treated rats than in controls ( P < 0.05). Dynamic compliance was also greater in Dex- and Dex + RA-treated rats than in controls or RA-treated rats ( P < 0.02). In Dex- and Dex + RA-treated rats, we observed increased hysteresis ratios ( P ≤ 0.006), air trapping ( P < 0.05), and lung volumes at 5 and 13.5 cmH2O pressure ( P < 0.001) and decreased elastic recoil ( P < 0.007). The effect of Dex on elastic recoil was greater in female than in male rats ( P = 0.006). Despite impaired septation, O2saturation was not compromised in Dex- or Dex + RA-treated rats. Thus lung function changes induced by Dex treatment during alveolarization were not prevented by concomitant treatment with RA.
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Honda, Y., H. Tani, A. Masuda, et al. "Effect of prior O2 breathing on ventilatory response to sustained isocapnic hypoxia in adult humans." Journal of Applied Physiology 81, no. 4 (1996): 1627–32. http://dx.doi.org/10.1152/jappl.1996.81.4.1627.
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Honda, Y., H. Tani, A. Masuda, T. Kobayashi, T. Nishino, H. Kimura, S. Masuyama, and T. Kuriyama. Effect of prior O2 breathing on ventilatory response to sustained isocapnic hypoxia in adult humans. J. Appl. Physiol. 81(4): 1627–1632, 1996.—Sixteen healthy volunteers breathed 100% O2 or room air for 10 min in random order, then their ventilatory response to sustained normocapnic hypoxia (80% arterial O2saturation, as measured with a pulse oximeter) was studied for 20 min. In addition, to detect agents possibly responsible for the respiratory changes, blood plasma of 10 of the 16 subjects was chemically analyzed. 1) Preliminary O2 breathing uniformly and substantially augmented hypoxic ventilatory responses. 2) However, the profile of ventilatory response in terms of relative magnitude, i.e., biphasic hypoxic ventilatory depression, remained nearly unchanged. 3) Augmented ventilatory increment by prior O2 breathing was significantly correlated with increment in the plasma glutamine level. We conclude that preliminary O2administration enhances hypoxic ventilatory response without affecting the biphasic response pattern and speculate that the excitatory amino acid neurotransmitter glutamate, possibly derived from augmented glutamine, may, at least in part, play a role in this ventilatory enhancement.
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Choi, Eun-Su, Jae-Hun Kim, Nam-Su Gil, et al. "Perioperative cerebral infarct during cardiac surgery and changes in jugular venous O2saturation and cerebral oximetry using near-infrared spectroscopy - A case report -." Korean Journal of Anesthesiology 56, no. 1 (2009): 102. http://dx.doi.org/10.4097/kjae.2009.56.1.102.
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Maryam, Yaghoubi Shahram Baraz* Mohammad Adineh Mohammad Hossain Haghighi zadeh. "THE EFFECT OF EXPIRATORY MANUAL RIB CAGE COMPRESSION BEFORE SUCTIONING ON BLOOD OXYGEN SATURATION IN PATIENTS." Indo American Journal of Pharmaceutical Sciences 04, no. 11 (2017): 4023–26. https://doi.org/10.5281/zenodo.1045212.
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Introduction: One of the most common ways put into practice to the clearance of the airway of patients who are under mechanical ventilation is applying suctioning into trachea. Some physiotherapeutic procedures including rib cage compression parallel to exhale and prior to suctioning can facilitate the egression of discharges. The present study aimed to determine the effect of rib cage compression during the exhale before suctioning on O2 saturation changes in patients receiving mechanical ventilation. Methodology: The research is a clinical trial study. The sample involved 55 patients who received mechanical ventilation hospitalized in special sections of health centers at Golestan and Emam-Khomeini hospitals in Ahvaz. The patients were divided into control and intervention groups by convenience sampling as paying attention to random involvement criteria. Blood oxygen saturation, within 5 minutes before and 15 and 25 minutes after suctioning were measured for intervention group using rib cage compression technique and the data were analyzed by independent t-test, and paired t-test as well as repeated measures design. Findings: The level of oxygen saturation increased by the trachea suctioning through rib cage compression technique and it is statistically meaningful at p< 0.05 . Conclusion: With respect to the improvement of blood oxygen saturation in intervention group, the technique is recommended for intubed patients. Keywords: Suctioning, compressing the rib cage, O2saturation, mechanical ventilation
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Carvalho, Clarissa Gutiérrez, Renato Soibelmann Procianoy, Eurico Camargo Neto, and Rita C. Silveira. "Preterm Neonates with Respiratory Distress Syndrome: Ventilator-Induced Lung Injury and Oxidative Stress." Journal of Immunology Research 2018 (2018): 1–4. http://dx.doi.org/10.1155/2018/6963754.
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Ventilator-induced lung injury is well recognized, and appropriate arterial saturation target is unknown, so gentle modes of ventilation and minimizing oxidative stress have been well studied. Our objective was to analyze any association between the oxygen levels at blood sampling and plasma levels of the interleukins IL-6, IL-1β, IL-10, and IL-8 and TNF-αin preterm newborns under mechanical ventilation (MV) in their first two days.Methods. Prospective cohort including neonates with severe respiratory distress. Blood samples were collected right before and 2 hours after invasive MV. For analysis purposes, newborns were separated according to oxygen requirement: low oxygen (≤30%) and high oxygen (>30%) groups. Interleukins were measured using a commercially available kit.Results. 20 neonates (gestational age 32.2 ± 3 weeks) were evaluated. Median O2saturation levels pre-MV were not different in both oxygen groups. In the high oxygen group, IL-6, IL-8, and TNF-αplasma levels increased significantly after two hours under MV.Conclusions. Despite the small sample studied, data showed that there is a relationship between VILI, proinflammatory cytokines, and oxygen-induced lung injury, but a study considering oxidative marker measurements is needed. It seems that less oxygen may keep safer saturation targets playing a less harmful role.
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Rurak, Dan, and Natalee W. Bessette. "Changes in fetal lamb arterial blood gas and acid-base status with advancing gestation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 304, no. 10 (2013): R908—R916. http://dx.doi.org/10.1152/ajpregu.00430.2012.
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To determine whether there are changes in blood gas and acid-base status with advancing gestation in the fetal lamb, similar to that reported in the human fetus, blood gas, acid-base, and blood metabolite values were measured in 447 control, arterial blood samples from 108 chronically instrumented fetal lambs between 103 and 146 days gestation. With advancing gestation, Po2, pH, O2saturation, and O2content fell significantly, while Pco2and hemoglobin concentration increased. Blood glucose and lactate concentrations were unchanged, although the lactate level increased with decreasing Po2, particularly when below ∼13 mmHg. Multiple linear regression indicated that increasing fetal number was associated with decreased Po2and glucose level and increased pH, HCO3−, base excess, and lactate concentration. Hemoglobin concentration was higher in female than male lambs. Overall, there was a linear relationship between glucose concentration and birth weight. It is concluded that in fetal lambs as in the human fetus, there are changes in blood gas and acid-base status with advancing gestation. This may be due to the decrease in fetal weight-normalized uterine and umbilical blood flows than occurs in these and other species as gestation proceeds. In addition, the reduced birth weight in twin and triplet lambs may be due to hypoglycemia rather than hypoxemia.
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Van Mil, Annette H. M., Aart Spilt, Mark A. Van Buchem, et al. "Nitric oxide mediates hypoxia-induced cerebral vasodilation in humans." Journal of Applied Physiology 92, no. 3 (2002): 962–66. http://dx.doi.org/10.1152/japplphysiol.00616.2001.
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Nitric oxide (NO) plays a pivotal role in the regulation of peripheral vascular tone. Its role in the regulation of cerebral vascular tone in humans remains to be elucidated. This study investigates the role of NO in hypoxia-induced cerebral vasodilatation in young healthy volunteers. The effect of the NO synthase inhibitor N G-monomethyl-l-arginine (l-NMMA) on the cerebral blood flow (CBF) was assessed during normoxia and during hypoxia (peripheral O2saturation 97 and 80%, respectively). Subjects were positioned in a magnetic resonance scanner, breathing normal air (normoxia) or a N2-O2 mixture (hypoxia). The CBF was measured before and after administration of l-NMMA (3 mg/kg) by use of phase-contrast magnetic resonance imaging techniques. Administration of l-NMMA during normoxia did not affect CBF. Hypoxia increased CBF from 1,049 ± 113 to 1,209 ± 143 ml/min ( P < 0.05). After l-NMMA administration, the augmented CBF returned to baseline (1,050 ± 161 ml/min; P < 0.05). Similarly, cerebral vascular resistance declined during hypoxia and returned to baseline after administration of l-NMMA ( P < 0.05 for both). Use of phase-contrast magnetic resonance imaging shows that hypoxia-induced cerebral vasodilatation in humans is mediated by NO.
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Takamura, Masayuki, Robert Parent, Peter Cernacek, and Michel Lavallée. "Influence of dual ETA/ETB-receptor blockade on coronary responses to treadmill exercise in dogs." Journal of Applied Physiology 89, no. 5 (2000): 2041–48. http://dx.doi.org/10.1152/jappl.2000.89.5.2041.
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We hypothesized that endothelin (ET) release during exercise may be triggered by α-adrenergic-receptor activation and thereby influence coronary hemodynamics and O2 metabolism in dogs. Exercise resulted in coronary blood flow increases (to 1.88 ± 0.26 from 1.10 ± 0.12 ml · min−1 · g−1) and in a fall ( P < 0.01) in coronary sinus O2saturation (17.4 ± 1.5 to 9.6 ± 0.7 vol%), whereas myocardial O2 consumption (MV˙o 2) increased (109 ± 13% from 145 ± 16 μl O2 · min−1 · g−1). Tezosentan, a dual ETA/ETB-receptor blocker, slightly reduced mean arterial pressure (MAP) and increased heart rate throughout exercise. The relationship between coronary sinus O2 saturation and MV˙o 2 was shifted upward ( P < 0.05) after tezosentan administration; i.e., as MV˙o 2 increased during exercise, coronary sinus O2 saturation was disproportionately higher after ET-receptor blockade. After propranolol, tezosentan resulted in significant decreases ( P < 0.05) in left ventricular pressure, the first derivative of left ventricular pressure over time, and MAP during exercise. As MV˙o 2 increased during exercise, coronary sinus O2 saturation levels after tezosentan became superimposable over those observed before ET-receptor blockade. Thus dual blockade of ETA/ETBreceptors alters coronary hemodynamics and O2 metabolism during exercise, but ET activity failed to increase beyond baseline levels.
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Zhang, Haibo, Giuliana Porro, Neil Orzech, Brendan Mullen, Mingyao Liu, and Arthur S. Slutsky. "Neutrophil defensins mediate acute inflammatory response and lung dysfunction in dose-related fashion." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 5 (2001): L947—L954. http://dx.doi.org/10.1152/ajplung.2001.280.5.l947.
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High concentrations of neutrophil defensins from airway and blood have been reported in patients with inflammatory lung diseases, but their exact role is unclear. We investigated the direct effect of defensins on the lungs of mice. Intratracheal instillation of purified defensins (5–30 mg/kg) induced a progressive reduction in peripheral arterial O2saturation, increased lung permeability, and enhanced the lung cytochrome c content. These indexes of acute lung dysfunction were associated with an increased total cell number and a significant neutrophil influx into the lung [5.1 ± 0.04% in control vs. 48.6 ± 12.7% in the defensin (30 mg/kg) group, P < 0.05]. Elastase concentrations in the bronchoalveolar lavage (BAL) fluids increased from 38 ± 11 ng/ml (control) to 80 ± 4 ng/ml (defensins, P < 0.05). Five hours after defensin instillation, concentrations of tumor necrosis factor- α and macrophage inflammatory protein-2 in BAL fluid were significantly increased. High levels of monocyte chemoattractant protein-1 in BAL fluid and plasma were also found after defensin stimulation. We conclude that intratracheal instillation of defensins causes acute lung inflammation and dysfunction, suggesting that high concentrations of defensins in the airways may play an important role in the pathogenesis of inflammatory lung diseases.
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Tzadok, Tomer, Ronen Toledano, Lior Fuchs, Carmi Bartal, Victor Novack, and Gal Ifergane. "Headache in the presentation of noncephalic acute illness." Journal of Neurosciences in Rural Practice 06, no. 04 (2015): 494–98. http://dx.doi.org/10.4103/0976-3147.168425.
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ABSTRACT Background: Headache is a frequent symptom of many systemic diseases that do not involve cranial structures. In this observational study, we assessed factors associated with headache in the acute presentation of systemic conditions in a nonsurgical emergency department (ED). Methods: Consecutive patients, admitted to Soroka University Medical Center ED due to noncephalic illness, were prospectively surveyed using a structured questionnaire focused on the prevalence and characteristics of headache symptoms. Medical data were extracted from the patient's charts. Results: Between 1 and 6/2012, 194 patients aged 64.69 ± 19.52 years, were evaluated. Headache was reported by 83 (42.7%) patients and was more common among patients with febrile illness (77.5% vs. 22.5%, P < 0.001). Respiratory illness and level of O2saturation were not associated with headache. Headache in the presentation of a noncephalic illness was associated with younger age (58 vs. 69, P < 0.001) and with suffering from a primary headache disorder (48.2% vs. 10.8%, P < 0.001). Headache was also associated with higher body temperature and lower platelets count. Conclusions: Headache is a common symptom in acute noncephalic conditions and was found to be associated with younger age and febrile disease on presentation. Patients who present with primary headache disorders are more prone to have headache during acute illness. Acute obstructive respiratory disease, hypercarbia or hypoxemia were not associated with headache.
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Vargas, Marco, Enrique Vargas, Colleen G. Julian, et al. "Determinants of blood oxygenation during pregnancy in Andean and European residents of high altitude." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 3 (2007): R1303—R1312. http://dx.doi.org/10.1152/ajpregu.00805.2006.
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High altitude decreases birth weight, but this effect is diminished in long vs. short-resident, high-altitude populations. We asked whether women from long vs. short-resident, high-altitude populations had higher arterial oxygenation levels by comparing 42 Andean and 26 European residents of La Paz, Bolivia (3,600 m), serially during pregnancy ( weeks 20, 30, and 36) and again 4 mo postpartum. Pregnancy raised hypoxic ventilatory sensitivity threefold, resting ventilation (V̇e), and arterial O2saturation (SaO2) in both groups. Ancestry, as identified using 81 genetic markers, correlated with respiratory pattern, such that greater Andean ancestry was associated with higher respiratory frequency and lower tidal volume. Pregnancy increased total blood and plasma volume ∼40% in both groups without changing red blood cell mass relative to body weight; hence, hemoglobin fell. The hemoglobin decline was compensated for by the rise in V̇e and SaO2with the result that arterial O2content (CaO2) was maintained near nonpregnant levels in both groups. Birth weights were similar for all Andean and European babies, but after adjusting for variation in gestational age, maternal height and parity, Andeans weighed 209 g more than Europeans. Babies with heavier birth weights and greater ponderal indices were born to Andean women with higher V̇e during pregnancy. We concluded that while maternal V̇e and arterial oxygenation were important, some factor other than higher CaO2was responsible for protecting Andeans from altitude-associated reductions in fetal growth.
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Nielsen, H. B., R. Boushel, P. Madsen, and N. H. Secher. "Cerebral desaturation during exercise reversed by O2 supplementation." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 3 (1999): H1045—H1052. http://dx.doi.org/10.1152/ajpheart.1999.277.3.h1045.
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The combined effects of hyperventilation and arterial desaturation on cerebral oxygenation ([Formula: see text]) were determined using near-infrared spectroscopy. Eleven competitive oarsmen were evaluated during a 6-min maximal ergometer row. The study was randomized in a double-blind fashion with an inspired O2 fraction of 0.21 or 0.30 in a crossover design. During exercise with an inspired O2 fraction of 0.21, the arterial CO2 pressure (35 ± 1 mmHg; mean ± SE) and O2 pressure (77 ± 2 mmHg) as well as the hemoglobin saturation (91.9 ± 0.7%) were reduced ( P < 0.05).[Formula: see text] was reduced from 80 ± 2 to 63 ± 2% ( P < 0.05), and the near-infrared spectroscopy-determined concentration changes in deoxy- (ΔHb) and oxyhemoglobin (ΔHbO2) of the vastus lateralis muscle increased 22 ± 3 μM and decreased 14 ± 3 μM, respectively ( P < 0.05). Increasing the inspired O2fraction to 0.30 did not affect ventilation (174 ± 4 l/min), but arterial CO2 pressure (37 ± 2 mmHg), O2 pressure (165 ± 5 mmHg), and hemoglobin O2saturation (99 ± 0.1%) increased ( P < 0.05).[Formula: see text] remained close to the resting level during exercise (79 ± 2 vs. 81 ± 2%), and although the muscle ΔHb (18 ± 2 μM) and ΔHbO2 (−12 ± 3 μM) were similar to those established without O2 supplementation, work capacity increased from 389 ± 11 to 413 ± 10 W ( P < 0.05). These results indicate that an elevated inspiratory O2fraction increases exercise performance related to maintained cerebral oxygenation rather than to an effect on the working muscles.
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Villafuerte, Francisco C., José Luis Macarlupú, Cecilia Anza-Ramírez, et al. "Decreased plasma soluble erythropoietin receptor in high-altitude excessive erythrocytosis and Chronic Mountain Sickness." Journal of Applied Physiology 117, no. 11 (2014): 1356–62. http://dx.doi.org/10.1152/japplphysiol.00619.2014.
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Excessive erythrocytosis (EE) is the hallmark of chronic mountain sickness (CMS), a prevalent syndrome in high-altitude Andean populations. Although hypoxemia represents its underlying stimulus, why some individuals develop EE despite having altitude-normal blood erythropoietin (Epo) concentration is still unclear. A soluble form of the Epo receptor (sEpoR) has been identified in human blood and competes directly for Epo with its membrane counterpart (mEpoR). Thus, reduced levels of circulating sEpoR could lead to higher Epo availability and ultimately to EE. We characterized the relationship between Epo and sEpoR, with hematocrit and hemoglobin concentration in healthy highlanders and CMS patients at 4,340 m in Cerro de Pasco, Peru. Our results show that EE patients show decreased plasma sEpoR levels and can be subdivided into two subgroups of normal and high plasma Epo concentration for the altitude of residence, with hemoglobin concentration rising exponentially with an increasing Epo-to-sEpoR ratio (Epo/sEpoR). Also, we showed that the latter varies as an inverse exponential function of arterial pulse O2saturation. Our findings suggests that EE is strongly associated with higher Epo/sEpoR values, leading to elevated plasma Epo availability to bind mEpoR, and thereby a stronger stimulus for augmented erythropoiesis. Differences in the altitude normal and high Epo CMS patients with a progressively higher Epo/sEpoR supports the hypothesis of the existence of two genetically different subgroups suffering from EE and possibly different degrees of adaptation to chronic high-altitude hypoxia.
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Hsia, Connie C. W., Robert L. Johnson, Eugene Y. Wu, Aaron S. Estrera, Harrieth Wagner, and Peter D. Wagner. "Reducing lung strain after pneumonectomy impairs oxygen diffusing capacity but not ventilation-perfusion matching." Journal of Applied Physiology 95, no. 4 (2003): 1370–78. http://dx.doi.org/10.1152/japplphysiol.00338.2003.
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After pneumonectomy (Pnx), mechanical strain on the remaining lung is an important signal for adaptation. To examine how mechanical lung strain alters gas exchange adaptation after Pnx, we replaced the right lung of adult dogs with a custom-shaped inflatable silicone prosthesis. The prosthesis was kept 1) inflated (Inf) to reduce mechanical strain of the remaining lung and maintain the mediastinum in the midline, or 2) deflated (Def) to allow lung strain and mediastinal shift. Gas exchange was studied 4-7 mo later at rest and during treadmill exercise by the multiple inert gas elimination technique while animals breathed 21 and 14% O2in balanced order. In the Inf group compared with Def group during hypoxic exercise, arterial O2saturation was lower and alveolar-arterial O2tension difference higher, whereas O2diffusing capacity was lower at any given cardiac output. Dispersion of the perfusion distribution was similar between groups at rest and during exercise. Dispersion of the ventilation distribution was lower in the Inf group at rest, associated with a much higher respiratory rate, but rose to similar levels in both groups during hypoxic exercise. Mean pulmonary arterial pressure at a given cardiac output was higher in the Inf group, whereas peak cardiac output was similar between groups. Thus creating lung strain by post-Pnx mediastinal shift primarily enhances diffusive gas exchange with only minor effects on ventilation-perfusion matching, consistent with the generation of additional alveolar-capillary surfaces but not conducting airways and blood vessels.
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Arabi, Yaseen, Barbara J. Morgan, Brian Goodman, Dominic S. Puleo, Ailiang Xie, and James B. Skatrud. "Daytime blood pressure elevation after nocturnal hypoxia." Journal of Applied Physiology 87, no. 2 (1999): 689–98. http://dx.doi.org/10.1152/jappl.1999.87.2.689.
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The purpose of this study was to investigate whether nocturnal hypoxia causes daytime blood pressure (BP) elevation. We hypothesized that overnight exposure to hypoxia leads the next morning to elevation in BP that outlasts the hypoxia stimulus. We studied the effect on BP of two consecutive night exposures to hypobaric hypoxia in 10 healthy normotensive subjects. During the hypoxia nights, subjects slept for 8 h in a hypobaric chamber at a simulated altitude of 4,000 m (barometric pressure = 462 mmHg). Arterial O2saturation and electrocardiogram were monitored throughout the night. For 30 min before the nocturnal simulated ascent and for 4 h after return to baseline altitude the next morning, BP was measured every 5 min while the subject was awake. The same measurements were made before and after 2 normoxic nights of sleep in the hypobaric chamber at ambient barometric pressure (745 mmHg). Principal components analysis was applied to evaluate patterns of BP response after the second night of hypoxia and normoxia. A distinct pattern of diastolic BP (DBP) elevation was observed after the hypoxia night in 9 of the 10 subjects but in none after the normoxia night. This pattern showed a mean increase of 4 mmHg in DBP compared with the presleep-awake baseline in the first 60 min and a return to baseline by 90 min. We conclude that nocturnal hypoxia leads to a carryover elevation of daytime DBP.
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Alecsandru, Diana, Israel Gestoso, Ana Romero, et al. "E. coliMultiresistant Meningitis after Transrectal Prostate Biopsy." Scientific World JOURNAL 6 (2006): 2323–26. http://dx.doi.org/10.1100/tsw.2006.362.
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Escherichia colimeningitis is a frequent pathology in children younger than 3 years old, but is an uncommon disease in adults.E. coliinfection is the main cause of intrahospital bacteremia as a consequence of the employment of different medical procedures. Our patient, male, 69 years old, presented with fever, progressive difficulty in breathing, and shivers 24 h after transrectal prostate biopsy, with an absence of any other symptoms. He received prophylactic treatment with ciprofloxacin and later empirical treatment with ampicillin and tobramicin. After that, the patient presented with fever, headache, behavioral changes, somnolence, disorientation, a fluctuating level of conscience, cutaneous widespread pallor, and acute urinary retention. On physical exploration, we observed generalized hypoventilation, Glasgow 10, stiffness of the neck, inconclusive Kernig; the remaining neurological exploration was normal. Systematic of blood: leukocytes = 8,510/mm3(94.5% polymorphonuclear), platelet = 87,000/mm3, pH = 7.51, pCO2= 28.8 mmHg, pO2= 61 mmHg, O2saturation = 93.8%, and remaining values were normal. Chest X- ray, cranial CT scan, urine cultures were normal. Blood culture:E. coli.CSF: glucose <0.4 g/l, total proteins = 3.05 g/l, PMN = 7 cells. Microscopic examination of the CSF: Gram-negative bacilli; CSF's culture: abundantE. coli.The case of acute meningitis by multiresistantE. coliafter transrectal prostate biopsy presented demonstrates that antibiotic prevention with ciprofloxacin is not absolutely risk free. Besides the use of antibiotic prevention for multiresistant microorganisms, the urologist and other physicians involved in the procedure must not forget that the rate of major complications of transrectal prostate biopsy is 1%, especially when it is performed in patients who will not benefit from that biopsy.
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Brutsaert, Tom D., Esteban J. Parra, Mark D. Shriver, et al. "Spanish genetic admixture is associated with larger V̇o2 maxdecrement from sea level to 4,338 m in Peruvian Quechua." Journal of Applied Physiology 95, no. 2 (2003): 519–28. http://dx.doi.org/10.1152/japplphysiol.01088.2002.
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Quechua in the Andes may be genetically adapted to altitude and able to resist decrements in maximal O2consumption in hypoxia (ΔV̇o2 max). This hypothesis was tested via repeated measures of V̇o2 max(sea level vs. 4,338 m) in 30 men of mixed Spanish and Quechua origins. Individual genetic admixture level (%Spanish ancestry) was estimated by using ancestry-informative DNA markers. Genetic admixture explained a significant proportion of the variability in ΔV̇o2 maxafter control for covariate effects, including sea level V̇o2 maxand the decrement in arterial O2saturation measured at V̇o2 max(ΔSpO2 max) ( R2for admixture and covariate effects ∼0.80). The genetic effect reflected a main effect of admixture on ΔV̇o2 max( P = 0.041) and an interaction between admixture and ΔSpO2 max( P = 0.018). Admixture predicted ΔV̇o2 maxonly in subjects with a large ΔSpO2 max( P = 0.031). In such subjects, ΔV̇o2 maxwas 12–18% larger in a subgroup of subjects with high vs. low Spanish ancestry, with least squares mean values (±SE) of 739 ± 71 vs. 606 ± 68 ml/min, respectively. A trend for interaction ( P = 0.095) was also noted between admixture and the decrease in ventilatory threshold at 4,338 m. As previously, admixture predicted ΔV̇o2 maxonly in subjects with a large decrease in ventilatory threshold. These findings suggest that the genetic effect on ΔV̇o2 maxdepends on a subject's aerobic fitness. Genetic effects may be more important (or easier to detect) in athletic subjects who are more likely to show gas-exchange impairment during exercise. The results of this study are consistent with the evolutionary hypothesis and point to a better gas-exchange system in Quechua.
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Ulatowski, John A., Enrico Bucci, Anna Razynska, Richard J. Traystman, and Raymond C. Koehler. "Cerebral blood flow during hypoxic hypoxia with plasma-based hemoglobin at reduced hematocrit." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 6 (1998): H1933—H1942. http://dx.doi.org/10.1152/ajpheart.1998.274.6.h1933.
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We determined whether cerebral blood flow (CBF) remained related to arterial O2 content ([Formula: see text]) during hypoxic hypoxia when hematocrit and hemoglobin concentration were independently varied with cell-free, tetramerically stabilized hemoglobin transfusion. Three groups of pentobarbital sodium-anesthetized cats were studied with graded reductions in arterial O2saturation to 50%: 1) a control group with a hematocrit of 31 ± 1% (mean ± SE; n = 7); 2) an anemia group with a hematocrit of 21 ± 1% that underwent an isovolumic exchange transfusion with an albumin solution ( n = 8); and 3) a group transfused with an intramolecularly cross-linked hemoglobin solution to decrease hematocrit to 21 ± 1% ( n = 10). Total arterial hemoglobin concentration (g/dl) after hemoglobin transfusion (8.8 ± 0.2) was intermediate between that of the control (10.3 ± 0.3) and albumin (7.2 ± 0.4) groups. Forebrain CBF increased after albumin and hemoglobin transfusion at normoxic O2 tensions to levels attained at equivalent reductions in [Formula: see text] in the control group during graded hypoxia. Over a wide range of arterial O2 saturation and sagittal sinus[Formula: see text], CBF remained greater in the albumin group. When CBF was plotted against[Formula: see text] for all three groups, a single relationship was formed. Cerebral O2 transport, O2 consumption, and fractional O2 extraction were constant during hypoxia and equivalent among groups. We conclude that CBF remains related to [Formula: see text] during hypoxemia when hematocrit is reduced with and without proportional reductions in O2-carrying capacity. Thus O2 transport to the brain is well regulated at a constant level independently of alterations in hematocrit, hemoglobin concentration, and O2 saturation.
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Chowdhuri, Susmita, Sukanya Pranathiageswaran, Rene Franco-Elizondo, et al. "Effect of age on long-term facilitation and chemosensitivity during NREM sleep." Journal of Applied Physiology 119, no. 10 (2015): 1088–96. http://dx.doi.org/10.1152/japplphysiol.00030.2015.
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The reason for increased sleep-disordered breathing with a predominance of central apneas in the elderly is unknown. We speculate that ventilatory control instability may provide a link between aging and the onset of unstable breathing during sleep. We sought to investigate potential underlying mechanisms in healthy, elderly adults during sleep. We hypothesized that there is 1) a decline in respiratory plasticity or long-term facilitation (LTF) of ventilation and/or 2) increased ventilatory chemosensitivity in older adults during non-, this should be hyphenated, non-rapid rapid eye movement (NREM) sleep. Fourteen elderly adults underwent 15, 1-min episodes of isocapnic hypoxia (EH), nadir O2saturation: 87.0 ± 0.8%. Measurements were obtained during control, hypoxia, and up to 20 min of recovery following the EH protocol, respectively, for minute ventilation (VI), timing, and inspiratory upper-airway resistances (RUA). The results showed the following. 1) Compared with baseline, there was a significant increase in VI(158 ± 11%, P < 0.05) during EH, but this was not accompanied by augmentation of VIduring the successive hypoxia trials nor in VIduring the recovery period (94.4 ± 3.5%, P = not significant), indicating an absence of LTF. There was no change in inspiratory RUAduring the trials. This is in contrast to our previous findings of respiratory plasticity in young adults during sleep. Sham studies did not show a change in any of the measured parameters. 2) We observed increased chemosensitivity with increased isocapnic hypoxic ventilatory response and hyperoxic suppression of VIin older vs. young adults during NREM sleep. Thus increased chemosensitivity, unconstrained by respiratory plasticity, may explain increased periodic breathing and central apneas in elderly adults during NREM sleep.
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Brutsaert, Tom D., Esteban J. Parra, Mark D. Shriver, Alfredo Gamboa, Maria Rivera-Ch, and Fabiola León-Velarde. "Ancestry explains the blunted ventilatory response to sustained hypoxia and lower exercise ventilation of Quechua altitude natives." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 1 (2005): R225—R234. http://dx.doi.org/10.1152/ajpregu.00105.2005.
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Andean high-altitude (HA) natives have a low (blunted) hypoxic ventilatory response (HVR), lower effective alveolar ventilation, and lower ventilation (VE) at rest and during exercise compared with acclimatized newcomers to HA. Despite blunted chemosensitivity and hypoventilation, Andeans maintain comparable arterial O2saturation (SaO2). This study was designed to evaluate the influence of ancestry on these trait differences. At sea level, we measured the HVR in both acute (HVR-A) and sustained (HVR-S) hypoxia in a sample of 32 male Peruvians of mainly Quechua and Spanish origins who were born and raised at sea level. We also measured resting and exercise VE after 10–12 h of exposure to altitude at 4,338 m. Native American ancestry proportion (NAAP) was assessed for each individual using a panel of 80 ancestry-informative molecular markers (AIMs). NAAP was inversely related to HVR-S after 10 min of isocapnic hypoxia ( r = −0.36, P = 0.04) but was not associated with HVR-A. In addition, NAAP was inversely related to exercise VE ( r = −0.50, P = 0.005) and ventilatory equivalent (VE/V̇o2, r = −0.51, P = 0.004) measured at 4,338 m. Thus Quechua ancestry may partly explain the well-known blunted HVR ( 10 , 35 , 36 , 57 , 62 ) at least to sustained hypoxia, and the relative exercise hypoventilation at altitude of Andeans compared with European controls. Lower HVR-S and exercise VE could reflect improved gas exchange and/or attenuated chemoreflex sensitivity with increasing NAAP. On the basis of these ancestry associations and on the fact that developmental effects were completely controlled by study design, we suggest both a genetic basis and an evolutionary origin for these traits in Quechua.
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Chen, Qiu-Hong, Ri-Li Ge, Xiao-Zhen Wang, et al. "Exercise performance of Tibetan and Han adolescents at altitudes of 3,417 and 4,300 m." Journal of Applied Physiology 83, no. 2 (1997): 661–67. http://dx.doi.org/10.1152/jappl.1997.83.2.661.
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Chen, Qiu-Hong, Ri-Li Ge, Xiao-Zhen Wang, Hui-Xin Chen, Tian-Yi Wu, Toshio Kobayashi, and Kazuhiko Yoshimura. Exercise performance of Tibetan and Han adolescents at altitudes of 3,417 and 4,300 m. J. Appl. Physiol. 83(2): 661–667, 1997.—The difference was studied between O2 transport in lifelong Tibetan adolescents and in newcomer Han adolescents acclimatized to high altitude. We measured minute ventilation, maximal O2 uptake, maximal cardiac output, and arterial O2 saturation during maximal exercise, using the incremental exercise technique, at altitudes of 3,417 and 4,300 m. The groups were well matched for age, height, and nutritional status. The Tibetans had been living at the altitudes for a longer period than the Hans (14.5 ± 0.2 vs. 7.8 ± 0.8 yr at 3,417 m, P < 0.01; and 14.7 ± 0.3 vs. 5.3 ± 0.7 yr at 4,300 m, P < 0.01, respectively). At rest, Tibetans had significantly greater vital capacity and maximal voluntary ventilation than the Hans at both altitudes. At maximal exercise, Tibetans compared with Hans had higher maximal O2 uptake (42.2 ± 1.7 vs. 36.7 ± 1.2 ml ⋅ min−1 ⋅ kg−1at 3,417 m, P < 0.01; and 36.8 ± 1.9 vs. 30.0 ± 1.4 ml ⋅ min−1 ⋅ kg−1at 4,300 m, P < 0.01, respectively) and greater maximal cardiac output (12.8 ± 0.3 vs. 11.4 ± 0.2 l/min at 3,417 m, P < 0.01; 11.5 ± 0.5 vs. 10.0 ± 0.5 l/min at 4,300 m, P < 0.05, respectively). Although the differences in arterial O2saturation between Tibetans and Hans were not significant at rest and during mild exercise, the differences became greater with increases in exercise workload at both altitudes. We concluded that exposure to high altitude from birth to adolescence resulted in an efficient O2 transport and a greater aerobic exercise performance that may reflect a successful adaptation to life at high altitude.
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Ge, Ri-Li, S. Witkowski, Y. Zhang, et al. "Determinants of erythropoietin release in response to short-term hypobaric hypoxia." Journal of Applied Physiology 92, no. 6 (2002): 2361–67. http://dx.doi.org/10.1152/japplphysiol.00684.2001.
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We measured blood erythropoietin (EPO) concentration, arterial O2saturation (SaO2), and urine Po2in 48 subjects (32 men and 16 women) at sea level and after 6 and 24 h at simulated altitudes of 1,780, 2,085, 2,454, and 2,800 m. Renal blood flow (Doppler) and Hb were determined at sea level and after 6 h at each altitude ( n = 24) to calculate renal O2delivery. EPO increased significantly after 6 h at all altitudes and continued to increase after 24 h at 2,454 and 2,800 m, although not at 1,780 or 2,085 m. The increase in EPO varied markedly among individuals, ranging from −41 to 400% after 24 h at 2,800 m. Similar to EPO, urine Po2decreased after 6 h at all altitudes and returned to baseline by 24 h at the two lowest altitudes but remained decreased at the two highest altitudes. Urine Po2was closely related to EPO via a curvilinear relationship ( r2= 0.99), although also with prominent individual variability. Renal blood flow remained unchanged at all altitudes. SaO2decreased slightly after 6 h at the lowest altitudes but decreased more prominently at the highest altitudes. There were only modest, albeit statistically significant, relationships between EPO and SaO2( r = 0.41, P < 0.05) and no significant relationship with renal O2delivery. These data suggest that 1) the altitude-induced increase in EPO is “dose” dependent: altitudes ≥2,100–2,500 m appear to be a threshold for stimulating sustained EPO release in most subjects; 2) short-term acclimatization may restore renal tissue oxygenation and restrain the rise in EPO at the lowest altitudes; and 3) there is marked individual variability in the erythropoietic response to altitude that is only partially explained by “upstream” physiological factors such as those reflecting O2delivery to EPO-producing tissues.
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Shoemaker, J. Kevin, Allen R. Kunselman, David H. Silber, and Lawrence I. Sinoway. "Maintained exercise pressor response in heart failure." Journal of Applied Physiology 85, no. 5 (1998): 1793–99. http://dx.doi.org/10.1152/jappl.1998.85.5.1793.
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The impact of forearm blood flow limitation on muscle reflex (metaboreflex) activation during exercise was examined in 10 heart failure (HF) (NYHA class III and IV) and 9 control (Ctl) subjects. Rhythmic handgrip contractions (25% maximal voluntary contraction, 30 contractions/min) were performed over 5 min under conditions of ambient pressure or with +50 mmHg positive pressure about the exercising forearm. Mean arterial blood pressure (MAP) and venous effluent hemoglobin (Hb) O2 saturation, lactate and H+ concentrations ([La] and [H+], respectively) were measured at baseline and during exercise. For ambient contractions, the increase (Δ) in MAP by end exercise (ΔMAP; i.e., the exercise pressor response) was the same in both groups (10.1 ± 1.2 vs. 7.33 ± 1.3 mmHg, HF vs. Ctl, respectively) despite larger Δ[La] and Δ[H+] for the HF group ( P < 0.05). With ischemic exercise, the ΔMAP for HF (21.7 ± 2.7 mmHg) exceeded that of Ctl subjects (12.2 ± 2.8 mmHg) ( P < 0.0001). Also, for HF, Δ[La] (2.94 ± 0.4 mmol) and Δ[H+] (24.8 ± 2.7 nmol) in the ischemic trial were greater than in Ctl (1.63 ± 0.4 mmol and 15.3 ± 2.8 nmol; [La] and [H+], respectively) ( P < 0.02). Hb O2 saturation was reduced in Ctl from ∼43% in the ambient trial to ∼27% with ischemia ( P < 0.0001). O2 extraction was maximized under ambient exercise conditions for HF but not for Ctl. Despite progressive increases in blood perfusion pressure over the course of ischemic exercise, no improvement in Hb O2saturation or muscle metabolism was observed in either group. These data suggest that muscle reflex activation of the pressor response is intact in HF subjects but the resulting improvement in perfusion pressure does not appear to enhance muscle oxidative metabolism or muscle blood flow, possibly because of associated increases in sympathetic vasoconstriction of active skeletal muscle.
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Wetter, Thomas J., Claudette M. St. Croix, David F. Pegelow, David A. Sonetti, and Jerome A. Dempsey. "Effects of exhaustive endurance exercise on pulmonary gas exchange and airway function in women." Journal of Applied Physiology 91, no. 2 (2001): 847–58. http://dx.doi.org/10.1152/jappl.2001.91.2.847.
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Seventeen fit women ran to exhaustion (14 ± 4 min) at a constant speed and grade, reaching 95 ± 3% of maximal O2 consumption. Pre- and postexercise lung function, including airway resistance [total respiratory resistance (Rrs)] across a range of oscillation frequencies, was measured, and, on a separate day, airway reactivity was assessed via methacholine challenge. Arterial O2saturation decreased from 97.6 ± 0.5% at rest to 95.1 ± 1.9% at 1 min and to 92.5 ± 2.6% at exhaustion. Alveolar-arterial O2 difference (A-aDo 2) widened to 27 ± 7 Torr after 1 min and was maintained at this level until exhaustion. Arterial Po 2 (PaO2 ) fell to 80 ± 8 Torr at 1 min and then increased to 86 ± 9 Torr at exhaustion. This increase in PaO2 over the exercise duration occurred due to a hyperventilation-induced increase in alveolar Po 2 in the presence of a constant A-aDo 2. Arterial O2 saturation fell with time because of increasing temperature (+2.6 ± 0.5°C) and progressive metabolic acidosis (arterial pH: 7.39 ± 0.04 at 1 min to 7.26 ± 0.07 at exhaustion). Plasma histamine increased throughout exercise but was inversely correlated with the fall in PaO2 at end exercise. Neither pre- nor postexercise Rrs, frequency dependence of Rrs, nor diffusing capacity for CO correlated with the exercise A-aDo 2 or PaO2 . Although several subjects had a positive or borderline hyperresponsiveness to methacholine, this reactivity did not correlate with exercise-induced changes in Rrs or exercise-induced arterial hypoxemia. In conclusion, regardless of the degree of exercise-induced arterial hypoxemia at the onset of high-intensity exercise, prolonging exercise to exhaustion had no further deleterious effects on A-aDo 2, and the degree of gas exchange impairment was not related to individual differences in small or large airway function or reactivity.
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Fernandes, Julia Freitas Rodrigues, Luciene da Silva Araújo, Sergio Emanuel Kaiser, Antonio Felipe Sanjuliani, and Márcia Regina Simas Torres Klein. "The effects of moderate energy restriction on apnoea severity and CVD risk factors in obese patients with obstructive sleep apnoea." British Journal of Nutrition 114, no. 12 (2015): 2022–31. http://dx.doi.org/10.1017/s0007114515004018.
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AbstractNutritional intervention for weight loss is one of the treatment options for obstructive sleep apnoea (OSA) in patients with overweight or obesity. However, the effects of moderate energy restriction on OSA severity are not yet known. The present study aimed to evaluate the effects of moderate energy restriction on OSA severity and CVD risk factors in obese patients with OSA. In this 16-week randomised clinical trial, twenty-one obese subjects aged 20–55 years and presenting an apnoea/hypopnoea index (AHI)≥5 events/h were randomised into two groups: the energy restriction group (ERG) and the control group (CG). The ERG was instructed to follow an energy-restricted diet −3347·2 kJ/d (−800 kcal/d) and the CG was advised not to change their food intake. At the beginning and at the end of the study, participants underwent evaluation of the following: OSA (Watch-PAT200®), nutritional parameters, blood pressure, sympathetic activity, inflammatory biomarkers, metabolic profile and endothelial function. The ERG (n11), compared with the CG (n10), had a significantly greater reduction in body weight (Cohen’sd=−1·19;P<0·001), in AHI (Cohen’sd=−0·95;P=0·04) and in plasma concentrations of adrenaline (Cohen’sd=−1·02;P=0·04) as well as a significantly greater increase in minimum O2saturation (Cohen’sd=1·08;P=0·03). Although energy restriction was not associated with significant improvements in CVD risk factors, medium-to-large effect sizes were observed, suggesting that the statistically non-significant difference between groups may be due to the small sample size. This study suggests that in obese patients with OSA, moderate energy restriction is able to reduce the parameters of OSA severity and sympathetic activity.
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Deacon, Naomi L., R. Doug McEvoy, Daniel L. Stadler, and Peter G. Catcheside. "Intermittent hypercapnic hypoxia during sleep does not induce ventilatory long-term facilitation in healthy males." Journal of Applied Physiology 123, no. 3 (2017): 534–43. http://dx.doi.org/10.1152/japplphysiol.01005.2016.
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Intermittent hypoxia-induced ventilatory neuroplasticity is likely important in obstructive sleep apnea pathophysiology. Although concomitant CO2levels and arousal state critically influence neuroplastic effects of intermittent hypoxia, no studies have investigated intermittent hypercapnic hypoxia effects during sleep in humans. Thus the purpose of this study was to investigate if intermittent hypercapnic hypoxia during sleep induces neuroplasticity (ventilatory long-term facilitation and increased chemoreflex responsiveness) in humans. Twelve healthy males were exposed to intermittent hypercapnic hypoxia (24 × 30 s episodes of 3% CO2and 3.0 ± 0.2% O2) and intermittent medical air during sleep after 2 wk washout period in a randomized crossover study design. Minute ventilation, end-tidal CO2, O2saturation, breath timing, upper airway resistance, and genioglossal and diaphragm electromyograms were examined during 10 min of stable stage 2 sleep preceding gas exposure, during gas and intervening room air periods, and throughout 1 h of room air recovery. There were no significant differences between conditions across time to indicate long-term facilitation of ventilation, genioglossal or diaphragm electromyogram activity, and no change in ventilatory response from the first to last gas exposure to suggest any change in chemoreflex responsiveness. These findings contrast with previous intermittent hypoxia studies without intermittent hypercapnia and suggest that the more relevant gas disturbance stimulus of concomitant intermittent hypercapnia frequently occurring in sleep apnea influences acute neuroplastic effects of intermittent hypoxia. These findings highlight the need for further studies of intermittent hypercapnic hypoxia during sleep to clarify the role of ventilatory neuroplasticity in the pathophysiology of sleep apnea.NEW & NOTEWORTHY Both arousal state and concomitant CO2levels are known modulators of the effects of intermittent hypoxia on ventilatory neuroplasticity. This is the first study to investigate the effects of combined intermittent hypercapnic hypoxia during sleep in humans. The lack of neuroplastic effects suggests a need for further studies more closely replicating obstructive sleep apnea to determine the pathophysiological relevance of intermittent hypoxia-induced ventilatory neuroplasticity.
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Modanlou, Houchang D., and Kay Beharry. "Biochemical and molecular endothelin responses to morphine sulfate infusion in conscious newborn piglets." Canadian Journal of Physiology and Pharmacology 76, no. 4 (1998): 443–50. http://dx.doi.org/10.1139/y98-034.
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The biochemical and molecular endothelin-1 (ET-1)responses to high dose morphine sulfate infusion were studied in conscious newborn piglets(n = 6) that received a loading dose of 100 µg/kg over 5 min followed by acontinuous i.v. infusion dose of 100 µg·kg1·h1 for 4 h. The controlgroup (n = 6) received equivalent volume loading and infusion doses of 5% dextrose.Blood samples were drawn serially from the femoral artery and sagittal sinus vein before (0),during (30 min, 1, 2, 3, and 4 h), and post (1 and 2 h) infusion. Five micrograms oftotal RNA obtained from brainstem tissue homogenates was analyzed by reverse transcriptase polymerase chain reaction (RT-PCR). The amounts of mRNA encoding ET-1, and endothelinreceptor subtypes ETA and ETB, were semiquantitated using densitometricscanning. Morphine infusion resulted in elevated respiratory rate and mean arterial bloodpressure, with no effect on arterial pH, PO2, and O2saturation. Compared with the control group, morphine induced significant elevations in plasmaET-1 levels following the bolus dose (systemic: 13.2 ± 3.6 vs. 8.6 ± 2.2 pg/mL, p < 0.05;sagittal sinus vein: 13.7 ± 3.4 vs. 8.2 ± 0.9 pg/mL, p < 0.01). These effects lasted up to2 h after discontinuation of morphine infusion (systemic: 14.5 ± 3.4 to 18.7 ± 5.7 pg/mL vs.7.5 ± 0.8 to 9.4 ± 3.2 pg/mL, p < 0.05 to p < 0.01; sagittal sinus vein: 14.8 ± 2.7to 17.6 ± 2.8 pg/mL vs. 7.5 ± 1.4 to 9.4 ± 3.4 pg/mL, p < 0.05 to p < 0.01). TheRT-PCR assay showed a twofold (p < 0.02) upregulation in ET-1 and a threefold(p < 0.007) upregulation in ETA receptor mRNA expression in the brainstemof morphine-treated animals. In contrast, there was a threefold (p < 0.0001)downregulation of the ETB receptor mRNA expression. The rapid and sustainedelevations in systemic arterial and sagittal sinus venous ET-1 levels suggest a role for ET-1 in themorphine-induced excitatory responses observed in newborn piglets. Upregulation ofETA receptors and downregulation of ETB receptors in the brainstem withhigh doses of morphine may indicate possible effects on cerebral vascular tone. Key words: morphine sulfate, endothelin-1, reverse transcriptase polymerase chain reaction.
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Wang, Winfred C., Molly Beth Freeman, Yvonne M. Carroll, et al. "High Failure Rate with Brigance Developmental Screening in 3 Year-Old Children with Sickle Cell Disease." Blood 124, no. 21 (2014): 4926. http://dx.doi.org/10.1182/blood.v124.21.4926.4926.
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Abstract Background: Central nervous system complications of sickle cell disease (SCD) include stroke, silent cerebral infarct, and neurocognitive deficits, but few studies have examined developmental delays in preschool-age children. Using the Brigance developmental screen in 3 year-old children with SCD we found a high frequency of scores below the “normal” cutoff for age, but control data were lacking (Ped. Blood Cancer 2011;56:620). We hypothesized that children with SCD would be more likely to “fail” this screening test than age-matched children from a similar ethnic/socio-economic background. Methods: This prospective study was approved by the St. Jude Children’s Research Hospital (SJCRH) IRB and informed consent obtained for each subject. 3.0-3.9 year-old SCD subjects were tested in the SJCRH Sickle Cell Clinic. Patients receiving chronic transfusion therapy were excluded. Age-matched and race-matched control subjects with similar socio-economic backgrounds were recruited from 8 Memphis daycare centers. The Brigance Preschool Screen was administered by trained examiners in the clinic or the daycare and required about 15 minutes to complete; the primary caretaker simultaneously completed the demographic form. None of the participants had previous exposure to the test. The proportions of subjects who failed the Brigance test (scoring below the age-related “cutoff”) and test raw scores (higher scores indicating better performance) were compared between SCD and control subjects using the exact Chi-square test and the two-sample t-test, respectively; logistic regression was used to model the associations between the Brigance failure proportions and other covariates for the groups. P-values <0.05 were considered significant. Results: Testing was performed on 103 SCD subjects not on treatment, an additional 20 HbSS subjects receiving hydroxyurea (HU), and 109 daycare subjects. Seventy-four percent of children with SCD (not on HU) failed the Brigance screen, compared to 61% of controls (p = 0.04). Mean (SD) Brigance raw scores for the non-HU SCD patients and controls were 45.9 (20.8) and 56.1 (22.5), respectively (p < 0.001). In the non-HU SCD group the pass/fail rate was not significantly different in those with more severe (SS, Sβ0thal) and milder (SC, Sβ+thal) genotypes. Medical factors, including absolute neutrophil count, hemoglobin concentration, %HbF level and O2saturation by pulse oximetry, were not associated with Brigance results. In contrast, socio-economic/demographic factors had a significant effect on the scores: lower income level, more household children under age 18, and more household residents were associated with increased failure (p </= 0.03). Lower caretaker education level showed a similar trend (p = 0.065). None of the socio-economic/demographic factors were associated with failure in the control group, although there was a trend toward failure with more household children under age 18 (p = 0.07). HU-treated SCD children were not significantly different from untreated patients in the failure rate (p = 0.4) and had no significant associations with medical or socio-economic factors. Conclusions: Among 3-year-olds tested with the Brigance Developmental Screen, a higher proportion of children with SCD failed compared to matched controls, but both groups showed a surprisingly high rate. Medical factors, such as hemoglobin level and sickle cell genotype, were not associated with the failure rate, nor was treatment with HU in a limited number of subjects. Socio-demographic factors (income level and numbers of household members) were associated with the failure rate in the SCD group, but not in the control group. These data indicate that preschool children with SCD are at very high risk for developmental delay, and underlying environmental factors seem to contribute more than medical factors. More detailed neurocognitive evaluation of preschool children with SCD and effective ways to enhance their development are needed. Disclosures Off Label Use: Hydroxyurea for children with sickle cell disease.
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Delmastro, M., C. Santoro, and S. Nava. "Respiratory changes during defecation in patients with chronic respiratory failure." March 24, 2004. https://doi.org/10.1183/09031936.04.00084504.
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Oxygen (O2) desaturation may occur in patients affected by respiratory diseases during daily activities, although most of these activities,e.g.walking, washing and cooking, can be avoided or eventually performed with an external aid.In this prospective study, the respiratory changes induced by the mandatory effort of defecation were assessed in patients with chronic respiratory insufficiency. Twenty-four consecutive patients with chronic respiratory failure due to obstructive or restrictive pulmonary disorders, showing a marked O2desaturation during the 6-min walk test, were enrolled. Thirteen of them were already established on long-term O2therapy (LTOT), while 11 were not. O2saturation (Sa,O2), respiratory rate (RR), cardiac frequency (fc) and dyspnoea were measured at rest, and during and after defecation.Sa,O2decreased significantly during defecation, while RR,fc and dyspnoea increased, both in the subgroup of patients without significant resting hypoxaemia and in the subgroup of patients receiving their usual resting flow of LTOT, as compared to resting values.In conclusion, the respiratory system of patients with chronic respiratory failure may be significantly strained by defecation.
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Griese, Matthias, Nicolaus Schwerk, Julia Carlens, et al. "Minimal important difference in childhood interstitial lung diseases." Thorax, December 26, 2022, thoraxjnl—2022–219206. http://dx.doi.org/10.1136/thorax-2022-219206.
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BackgroundMonitoring disease progression in childhood interstitial lung diseases (chILD) is essential. No information for the minimal important difference (MID), which is defined as the smallest change in a parameter that is perceived as important prompting a clinician to change the treatment, is available. We calculated MIDs for vital signs (respiratory rate, peripheral oxygen saturation in room air, Fan severity score) and health-related quality of life (HrQoL) scores.MethodsThis study used data from the Kids Lung Register, which is a web-based management platform that collects data of rare paediatric lung disorders with a focus on chILD. Data of vital signs and HrQoL scores (Health Status Questionnaire, chILD-specific questionnaire and PedsQL V.4.0) were collected. MIDs were calculated according to distribution-based (one-third SD) and anchor-based methods (using forced expiratory volume in 1 s and forced vital capacity) as anchors.ResultsBaseline data of 774 children were used to calculate the following MIDs: respiratory rate 1.3 (z-score), O2saturation in room air 3.0%, Fan severity score 0.2–0.4, Health Status Questionnaire 0.4–0.8, chILD-specific questionnaire 4.4%–8.2%, physical health summary score 7.8%–8.9%, psychosocial health summary score 3.4%–6.9% and total score 5.1%–7.4%. Results of the responsiveness analysis generally agreed with the MIDs calculated.ConclusionsFor the first time, we provide estimates of MIDs for vital signs and HrQoL scores in a large cohort of chILD using different methods.
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Langer, Christine, Claus Wittekindt, Christoph Arens, and Sonja Käbisch. "Apnoeic oxygenation with high flow nasal oxygen for interventional surgery of the larynx and pharynx." European Archives of Oto-Rhino-Laryngology, May 16, 2024. http://dx.doi.org/10.1007/s00405-024-08726-6.
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Abstract Background Highflow nasal cannula oxygen (HFNO) is known to be used for noninvasive oxygenation in intensive care patients but it has rarely been used in airway management for elective surgery of the upper aerodigestive tract. Objectives HFNO offers opportunities of a tubeless oxygenation system which is easy to handle and not limited only on surgery of the endolarynx. Methods We evaluated this method for oxygenation during brief interventional procedures of the larynx and pharynx in 92 adult patients for safety and intraoperative complications. The need of secondary endotracheal intubation and limiting comorbidities as pulmonal and cardiac diseases were documented. Results HFNO showed a good safety profile concerning saturation and hypercapnia. Oxygen desaturation below 90% occurred only in 5 patients, mask ventilation led to quick recovery except in one patient who was secondary intubated. A significant influence of the body mass index on the minimal O2 saturation was shown (p < 0,001) so that a possible limitation of the method exists here. Comorbidities were grouped into the ASA classification. There was a significant difference between ASA I/II and ASA III patients in terms of minimum O2saturation. Conclusion We conclude that HFNO may hold great promise for changing ventilator technique in general anesthesia, particularly in short elective laryngeal and pharyngeal surgery. Safety and feasibility were proven in this study.
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Pereira da Silva Carpeggiani, Fernanda, Thiago Menezes Cézar, Tatiana Schäffer Gregianini, Felipe Grillo Pinheiro, Letícia Garay Martins, and Ana Beatriz Gorini da Veiga. "Impact of COVID-19 on the epidemiology of respiratory viruses in southern Brazil." Revista de Epidemiologia e Controle de Infecção 14, no. 2 (2024). http://dx.doi.org/10.17058/reci.v14i2.18935.
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Background and objectives: During the SARS-CoV-2 pandemic, reduction in detection of other Respiratory Viruses (RV) was observed. Epidemiological studies are needed to understand the impact of the pandemic on the circulation of RV. The aim of this study is to analyze the epidemiological profile of cases of severe acute respiratory infection (SARI) associated with the main RV in hospitalized patients from RS, between 2010 and 2019 (period A) and between 2020 and 2021 (period B). Methods: Data related to SARI cases in RS were retrieved from SIVEP-Gripe. Results: In period A there were more infections with Influenza, Parainfluenza, Adenovirus and Respiratory Syncytial Virus, while in period B most cases were of SARS-CoV-2 infection. The most affected age groups were individuals <5 years old (67.1%) in period A, and >60 years old (50%) in period B. The main symptoms were fever and cough in period A, and dyspnea and O2saturation <95% in period B. The most reported comorbidities were lung diseases and chronic cardiovascular diseases in period A, and chronic cardiovascular diseases and diabetes mellitus in period B. Importantly, a higher fatality rate was observed in period B. Most cases occurred between May and July in period A, and in November and December 2021 in period B. Conclusion: This study reveals that the COVID-19 pandemic changed the epidemiological profile of SARI in RS, and most cases were in the elderly with chronic cardiovascular disease and diabetes mellitus.