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Belyayeva, V. A. "The impact of meteo-factors on increase of arterial blood pressure." Health Risk Analysis, no. 4 (April 2016): 17–22. http://dx.doi.org/10.21668/health.risk/2016.4.02.eng.
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Coral-Alvarado, Paola Ximena, Maria Fernanda Garces, Jorge Eduardo Caminos, Antonio Iglesias-Gamarra, José Félix Restrepo, and Gerardo Quintana. "Serum Endoglin Levels in Patients Suffering from Systemic Sclerosis and Elevated Systolic Pulmonary Arterial Pressure." International Journal of Rheumatology 2010 (2010): 1–6. http://dx.doi.org/10.1155/2010/969383.
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Background. Pulmonary arterial hypertension (PAH) is the main cause of morbimortality in systemic sclerosis (SSc). Increased Eng expression has been demonstrated in SSc patients.Objective. Ascertaining serum levels of Eng in SSc patients with and without elevated systolic pulmonary arterial pressure (sPAP) and comparing them with that of healthy volunteers.Methods. A cross-sectional study was carried out. A commercial ELISA kit was used for measuring serum concentrations of Eng in 60 subjects: 40 patients with SSc with and without elevated sPAP, compared to 20 healthy control subjects. Elevated sPAP was detected by echocardiogram.Results. No association between positive Eng and elevated sPAP was found when compared to the SSc without elevated sPAP group (OR=2.85; 0.65–12.88 95% CI;P=.11); however, an association was found between positive Eng and elevated sPAP compared to healthy controls (OR=23.22; 2.46–1050.33 95% CI;P=.001), and weak association was found between the positive Eng with SSc without elevated sPAP group compared to healthy controls (OR=8.14, 0.8–393.74 95% CI;P=.046).Conclusion. Raised serum levels of Eng in SSc patients compared to healthy controls were found, suggesting a role for Eng in SSc vasculopathy and not just in elevated sPAP. However, prospective studies are needed to verify such observations.
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Tas, Umit, and Ahmet Akbas. "ANFIS Based Modeling of the Hormonal Effects of GLP-2 on the Mean Arterial Pressure and Blood Volume of Rats." مجلة جامعة الملك عبدالعزيز-العلوم الهندسية 25, no. 1 (2014): 21–32. http://dx.doi.org/10.4197/eng.25-1.2.
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Umnyagina, I. A., T. V. Blinova, L. A. Strakhova, V. V. Troshin, Yu V. Ivanova, and E. I. Sorokina. "Endothelin-1 as a risk factor causing cardiovascular pathology in young and middle-aged people employed under hazardous working conditions." Health Risk Analysis, no. 2 (June 2021): 105–13. http://dx.doi.org/10.21668/health.risk/2021.2.10.eng.
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Our research goal was to reveal peculiarities related to changes in endothelin-1 contents in blood serum in young and middle-aged people exposed to occupational noise and industrial welding and silicon-containing aerosols with fibrogenic effects. Another goal was to establish a correlation between endothelin-1 contents and blood pressure, body mass, and dyslipidemia. We examined workers employed at a metallurgic plant in Nizhniy Novgorod region. Endothelin-1 concentration in blood serum was determined with «Endothelin (1-21)», a reagent kit for ELISA produced by «Biomedica Medizinprodukte GmbH & Co KG» (Austria). We detected certain group differences in endothelin-1 contents in blood serum and frequency of its elevated concentrations between workers who had to work under different working conditions. We established a direct correlation between endothelin-1 and blood pressure, total cholesterol, and body mass index. Elevated endothelin-1 contents in people suffering from arterial hypertension can indicate a higher risk of complications this disease might have. People who have elevated endothelin-1 contents but normal blood pressure, total cholesterol within physiological standard and normal body mass index can be recommended to have regular medical check-ups focusing on functional state of their cardiovascular system; endothelin-1 in this case should be considered a risk factor that might cause cardiovascular pathology occurrence. An individual approach is required when assessing elevated endothelin-1 contents and probable use of this parameter as a risk factor that might cause cardiovascular pathology in young and middle-aged people employed under hazardous working conditions.
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Weese-Mayer, D. E., R. T. Brouillette, L. Klemka, and C. E. Hunt. "Effects of almitrine on hypoglossal and phrenic electroneurograms." Journal of Applied Physiology 59, no. 1 (July 1, 1985): 105–12. http://dx.doi.org/10.1152/jappl.1985.59.1.105.
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Almitrine increases breathing by stimulating peripheral chemoreceptors. Previous studies suggest clinical usefulness in the adult with chronic obstructive pulmonary disease, but little data are available to decide whether almitrine would be helpful in diseases involving pharyngeal airway obstruction, such as apnea of prematurity or obstructive sleep apnea. We investigated the effect of intravenous almitrine on hypoglossal (HG), an upper airway nerve, and phrenic (PHR) neural activity in eight alpha-chloralose-urethan anesthetized, paralyzed, vagotomized, and artificially ventilated cats. Recordings were made of raw and integrated HG and PHR electroneurograms (ENGs), alveolar PCO2, arterial PO2, arterial blood pressure, and rectal temperature. A dose-response study of cumulative almitrine doses ranging from 0.1 to 4.0 mg/kg was performed in three cats. The interactive effects of almitrine and hypoxic stimulation were investigated in four cats. The interactive effects of almitrine and hypercapnic stimulation were investigated in five cats. The interactive effects of almitrine and ventilatory timing were investigated in six cats. We found that 1) almitrine doses as low as 0.1 mg/kg iv increased both HG and PHR ENG activity, with a maximum effect at approximately 1.0 mg/kg; 2) almitrine markedly increased HG and PHR ENG activity at all arterial PO2 values from 35–175 Torr; 3) almitrine increased HG and PHR ENG activity at all arterial PCO2 values from 30–70 Torr; and 4) almitrine increased the ratio of tidal volume to inspiratory time and decreased the inspiratory muscle duty cycle at normoxia and eucapnia.
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Tsamis, Alkiviadis, and Nikos Stergiopulos. "Arterial remodeling in response to hypertension using a constituent-based model." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 5 (November 2007): H3130—H3139. http://dx.doi.org/10.1152/ajpheart.00684.2007.
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Hypertension-induced arterial remodeling has been previously modeled using stress-driven remodeling rate equations in terms of global geometrical adaptation (Rachev A, Stergiopulos N, Meister JJ. Theoretical study of dynamics of arterial wall remodeling in response to changes in blood pressure. J Biomech 29: 635–642, 1996) and was extended later to include adaptation of material properties (Rachev A, Stergiopulos N, Meister JJ. A model for geometric and mechanical adaptation of arteries to sustained hypertension. J Biomech Eng 120: 9–17, 1998). These models, however, used a phenomenological strain energy function (SEF), the parameters of which do not bear a clear physiological meaning. Here, we extend the work of Rachev et al. (1998) by applying similar remodeling rate equations to a constituent-based SEF. The new SEF includes a statistical description for collagen engagement, and remodeling now affects material properties only through changes in the collagen engagement probability density function. The model predicts asymptotic wall thickening and unchanged deformed inner radius as to conserve hoop stress and intimal shear stress, respectively, at the final adapted hypertensive state. Mechanical adaptation serves to restore arterial compliance to control levels. Average circumferential stress-strain curves show that the material at the final adapted hypertensive state is softer than its normotensive counterpart. These findings as well as the predicted pressure-diameter curves are in good qualitative agreement with experimental data. The novelty in our findings is that biomechanical adaptation leading to maintenance of compliance at the hypertensive state can be perfectly achieved by appropriate readjustment of the collagen engagement profile alone.
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Fan, Wei, and Michael C. Andresen. "Differential frequency-dependent reflex integration of myelinated and nonmyelinated rat aortic baroreceptors." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 2 (August 1, 1998): H632—H640. http://dx.doi.org/10.1152/ajpheart.1998.275.2.h632.
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Electrical activation of myelinated (A type) and nonmyelinated (C type) baroreceptor axons (BR) in aortic depressor nerve (ADN) evoked baroreflex changes in mean arterial pressure (MAP) in chloralose-urethan-anesthetized rats. Low stimulation intensities (<3 V) activated only A-type BR electroneurograms (ENG). A-type selective stimulus trains required minimum frequencies >10 Hz to evoke reflex MAP decreases, and the largest MAP responses occurred at 50 Hz and higher. In contrast, high stimulation intensities (18–20 V) maximally activated two volleys in ADN ENG corresponding to A- and C-type BR volleys. High-intensity trains decreased MAP at low frequency (1 Hz) and largest reflex responses at ≥5 Hz. Capsaicin (Cap) applied periaxonally to ADN selectively blocked C-type ENG volleys but not A-type volleys. Reflex curves with supramaximal intensity during Cap were indistinguishable from the pre-Cap, low-intensity baroreflexes. In comparison, vagus ENG showed graded Cap block of the C-fiber volley (ED50 = 200 nM) without significant attenuation of the A-type volley below 1 μM. However, 100 μM Cap blocked conduction in all myelinated vagal axons as well as C-type axons. Thus Cap is selective for sensory C-type axons only at low micromolar concentrations. Myelinated and nonmyelinated arterial BR evoke characteristically different frequency-response reflex relations that suggest distinct differences in sensory information processing mechanisms.
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SARIFUDDIN, SANTABRATA CHAKRAVARTY, and PRASHANTA KUMAR MANDAL. "EFFECT OF ASYMMETRY AND ROUGHNESS OF STENOSIS ON NON-NEWTONIAN FLOW PAST AN ARTERIAL SEGMENT." International Journal of Computational Methods 06, no. 03 (September 2009): 361–88. http://dx.doi.org/10.1142/s0219876209001887.
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Numerical investigations of non-Newtonian blood flow are carried out through an asymmetric arterial constriction (stenosis) obtained from casting of mildly stenosed artery [Back et al. [1984] Effect of mild atherosclerosis on flow resistance in a coronary artery casting by man, J. Biomech. Eng., Trans. ASME106, 48]. The Marker and Cell method, for governing equations of motion for the flow in primitive variables formulations is developed in a staggered grid to discretize the momentum equations representing the non-Newtonian viscous incompressible flow characterized by the generalized Power-law model in cylindrical coordinates system under axial symmetric conditions so that the problem effectively becomes two-dimensional. The modified pressure equation has been solved by Successive-Over-Relaxation method and the pressure–velocity correction formulae have been derived. Satisfactory level of convergence namely, the mass conservation of the order of 0.5 × 10-12 and consequently the steady-state criteria have been achieved. The separation points, reattachment points, pressure drop, and the wall shear stress distribution resulting from the present simulation agree well with the available numerical and experimental results. Secondary separation has also been predicted at higher Reynolds numbers. Further, in-depth study of the flow patterns reveals that shear-thickening model of generalized Power-law fluid experiences excess pressure drop more than that of shear-thinning model as in the case of flow past through cosine and smooth-shaped constrictions than irregular ones. The efficiency of the numerical code is illustrated by applying it to a test problem in order to validate the applicability of the technique as well as the simulation under consideration.
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Bofarid, Sala, Anna E. Hosman, Johannes J. Mager, Repke J. Snijder, and Marco C. Post. "Pulmonary Vascular Complications in Hereditary Hemorrhagic Telangiectasia and the Underlying Pathophysiology." International Journal of Molecular Sciences 22, no. 7 (March 27, 2021): 3471. http://dx.doi.org/10.3390/ijms22073471.
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In this review, we discuss the role of transforming growth factor-beta (TGF-β) in the development of pulmonary vascular disease (PVD), both pulmonary arteriovenous malformations (AVM) and pulmonary hypertension (PH), in hereditary hemorrhagic telangiectasia (HHT). HHT or Rendu-Osler-Weber disease is an autosomal dominant genetic disorder with an estimated prevalence of 1 in 5000 persons and characterized by epistaxis, telangiectasia and AVMs in more than 80% of cases, HHT is caused by a mutation in the ENG gene on chromosome 9 encoding for the protein endoglin or activin receptor-like kinase 1 (ACVRL1) gene on chromosome 12 encoding for the protein ALK-1, resulting in HHT type 1 or HHT type 2, respectively. A third disease-causing mutation has been found in the SMAD-4 gene, causing a combination of HHT and juvenile polyposis coli. All three genes play a role in the TGF-β signaling pathway that is essential in angiogenesis where it plays a pivotal role in neoangiogenesis, vessel maturation and stabilization. PH is characterized by elevated mean pulmonary arterial pressure caused by a variety of different underlying pathologies. HHT carries an additional increased risk of PH because of high cardiac output as a result of anemia and shunting through hepatic AVMs, or development of pulmonary arterial hypertension due to interference of the TGF-β pathway. HHT in combination with PH is associated with a worse prognosis due to right-sided cardiac failure. The treatment of PVD in HHT includes medical or interventional therapy.
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Bouwmeester, J. Christopher, Israel Belenkie, Nigel G. Shrive, and John V. Tyberg. "Partitioning pulmonary vascular resistance using the reservoir-wave model." Journal of Applied Physiology 115, no. 12 (December 15, 2013): 1838–45. http://dx.doi.org/10.1152/japplphysiol.00750.2013.
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The conventional determination of pulmonary vascular resistance does not indicate which vascular segments contribute to the total resistance of the pulmonary circulation. Using measurements of pressure and flow, the reservoir-wave model can be used to partition total pulmonary vascular resistance into arterial, microcirculation, and venous components. Changes to these resistance components are investigated during hypoxia and inhaled nitric oxide, volume loading, and positive end-expiratory pressure. The reservoir-wave model defines the pressure of a volume-related reservoir and the asymptotic pressure. The mean values of arterial and venous reservoir pressures and arterial and venous asymptotic pressures define a series of resistances between the main pulmonary artery and the pulmonary veins: the resistance of large and small arteries, the microcirculation, and veins. In 11 anaesthetized, open-chest dogs, pressure and flow were measured in the main pulmonary artery and a single pulmonary vein. Volume loading reduced each vascular resistance component, whereas positive end-expiratory pressure only increased microcirculation resistance. Hypoxia increased the resistance of small arteries and veins, whereas nitric oxide only decreased small-artery resistance significantly. The reservoir-wave model provides a novel method to deconstruct total pulmonary vascular resistance. The results are consistent with the expected physiological responses of the pulmonary circulation and provide additional information regarding which segments of the pulmonary circulation react to hypoxia and nitric oxide.
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DATIR, PARAG, AVIONE Y. LEE, SHAWN D. LAMM, and HAI-CHAO HAN. "EFFECTS OF GEOMETRIC VARIATIONS ON THE BUCKLING OF ARTERIES." International Journal of Applied Mechanics 03, no. 02 (June 2011): 385–406. http://dx.doi.org/10.1142/s1758825111001044.
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Arteries often demonstrate geometric variations such as elliptic and eccentric cross sections, stenosis, and tapering along the longitudinal axis. Effects of these variations on the mechanical stability of the arterial wall have not been investigated. The objective of this study was to determine the buckling behavior of arteries with elliptic, eccentric, stenotic, and tapered cross sections. The arterial wall was modeled as a homogeneous anisotropic nonlinear material. Finite element analysis was used to simulate the buckling process of these arteries under lumen pressure and axial stretch. Our results demonstrated that arteries with an oval cross section buckled in the short axis direction at lower critical pressures as compared to circular arteries. Eccentric cross sections, stenosis, and tapering also decreased the critical pressure. Stenosis led to dramatic pressure variations along the vessel and reduced the buckling pressure. In addition, tapering shifted the buckling deformation profile of the artery towards the distal end. We conclude that geometric variations reduce the critical pressure of arteries and thus make the arteries more prone to mechanical instability than circular cylindrical arteries. These results improve our understanding of the mechanical behavior of arteries.
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Pimpare, Dr Meena M. "Correlation between End-Tidal Carbon Dioxide Pressure and Arterial Carbon Dioxide Partial Pressure in Patients Undergoing Craniotomy." Journal of Medical Science And clinical Research 05, no. 03 (March 7, 2017): 18525–33. http://dx.doi.org/10.18535/jmscr/v5i3.43.
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Kelly, S. M., A. E. Taylor, and R. P. Michel. "Bronchial collateral vessel micropuncture pressure in postobstructive pulmonary vasculopathy." Journal of Applied Physiology 73, no. 5 (November 1, 1992): 1914–24. http://dx.doi.org/10.1152/jappl.1992.73.5.1914.
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Postobstructive pulmonary vasculopathy, produced by chronic ligation of one pulmonary artery, markedly increases bronchial blood flow. Previously, using arterial and venous occlusion, we determined that bronchial collaterals enter the pulmonary circuit at the distal end of the arterial segment. In this study, we tested the hypothesis that pressure in bronchial collaterals (Pbr) closely approximates that at the downstream end of the arterial segment (Pao). We pump perfused [111 +/- 10 (SE) ml/min] left lower lobes of seven open-chest live dogs 3–15 mo after ligation of the left main pulmonary artery. Bronchial blood flow was 122 +/- 16 ml/min. We measured pulmonary arterial and venous pressures and, by arterial and venous occlusion, respectively, Pao and the pressure at the upstream end of the venous segment (Pvo). Pbr was obtained by micropuncture of 34 pleural surface bronchial vessels 201 +/- 16 microns in diameter. We found that Pbr (14.4 +/- 1.0 mmHg) was similar to Pao (15.0 +/- 0.8 mmHg) but differed significantly (P < 0.01) from Pvo (11.3 +/- 0.5 mmHg). In addition, Pbr was independent of systemic arterial pressure and bronchial vessel diameter. Light and electron microscopy revealed that, in the lobes with the ligated pulmonary artery, the new bronchial collaterals entered the thickened pleura from the parenchyma via either bronchovascular bundles or interlobular septa and had sparsely muscularized walls. We conclude that, in postobstructive pulmonary vasculopathy, bronchial collateral pressure measured by micropuncture is very close to the pressure in precapillary pulmonary arteries and that most of the pressure drop in the bronchial collaterals occurs in vessels > 350 microns in diameter.
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Seaworth, J. F., T. J. Jennings, L. L. Howell, J. W. Frazier, C. D. Goodyear, and E. D. Grassman. "Hemodynamic effects of anti-G suit inflation in a 1-G environment." Journal of Applied Physiology 59, no. 4 (October 1, 1985): 1145–51. http://dx.doi.org/10.1152/jappl.1985.59.4.1145.
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This study evaluated effects of various anti-G inflation pressures on cardiac volumes and the relationship of these volume changes to mean arterial pressure changes. Ventricular volumes were calculated using two-dimensional echocardiography. An anti-G suit was inflated to 2, 4, and 6 psi in the standing and supine positions for 10 male subjects. In the supine position, mean arterial pressure increased from base line for all three inflation pressures (P = 0.05). The end-diastolic volume increased after 2-psi inflation (P = 0.03). Cardiac output or stroke volume did not change. After standing, mean arterial pressure (P = 0.002), end-diastolic volume (P = 0.002), and stroke volume (P = 0.05) fell after suit deflation. Peripheral vascular resistance fell in the 2- and 4-psi inflation profiles. In the standing protocol, mean arterial pressure, end-diastolic volume, stroke volume, and cardiac output rose with all three inflation pressures (P less than 0.05). After reclining, heart rate increased (P = 0.02) and mean arterial pressure fell (P less than 0.05) in the 4- and 6-psi inflation profiles after suit deflation. Increases in mean arterial pressure are caused by increases in cardiac preload and cardiac output after inflation of the anti-G suit while subjects were standing. Increased cardiac preload was not consistently seen after inflation while subjects were supine. Changes in end-diastolic volume and mean arterial pressure were dependent on the pressure used to inflate the anti-G suit.
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Graham, Eric M., Andrew M. Atz, Scott M. Bradley, Mark A. Scheurer, Varsha M. Bandisode, Antonio Laudito, and Girish S. Shirali. "Does a ventriculotomy have deleterious effects following palliation in the Norwood procedure using a shunt placed from the right ventricle to the pulmonary arteries?" Cardiology in the Young 17, no. 2 (January 23, 2007): 145–50. http://dx.doi.org/10.1017/s1047951107000133.
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Introduction: A recent modification to the Norwood procedure involving a shunt placed directly from the right ventricle to the pulmonary arteries may improve postoperative haemodynamics. Concerns remain, however, about the potential problems produced by the required ventriculotomy. Methods: We compared 76 patients with hypoplastic left heart syndrome who underwent the Norwood procedure, 35 receiving a modified Blalock-Taussig shunt and the remaining 41 a shunt placed directly from the right ventricle to the pulmonary arteries. We reviewed their subsequent progress through the second stage of palliation. A single observer graded right ventricular function, and the severity of tricuspid regurgitation, based on blinded review of the most recent echocardiograms prior to the second stage of palliation. Results: At the time of catheterization prior to the second stage, patients with a shunt placed from the right ventricle to the pulmonary arteries, rather than a modified Blalock-Taussig shunt, had higher arterial diastolic blood pressure, at 44 versus 40 millimetres of mercury, p equal to 0.02, lower ventricular end diastolic pressures, at 8 versus 11 millimetres of mercury, p equal to 0.0002, and larger pulmonary arteries as judged using the Nakata index, at 270 versus 188 millimetres squared per metres squared, p equal to 0.009. There was no difference in qualitative ventricular systolic function or tricuspid regurgitation between groups. No differences were found between groups during the hospitalization following the second stage of palliation. A trend towards improved survival to the second stage was seen following the construction of a shunt from the right ventricle to the pulmonary arteries. Conclusions: Construction of a shunt from the right ventricle to the pulmonary arteries is associated with lower right ventricular end diastolic pressures, larger pulmonary arterial size, and higher systemic arterial diastolic pressures. No apparent deleterious effects of the right ventriculotomy were observed in terms of qualitative ventricular systolic function or tricuspid regurgitation.
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Tozzi, Hayoz, Mueller, M'Baku, Mallabiabarrena, and von Segesser. "Anastomotic Longitudinal Stress due to Modification of Arterial Longitudinal Properties after Anastomosis." Swiss Surgery 6, no. 2 (April 1, 2000): 74–76. http://dx.doi.org/10.1024/1023-9332.6.2.74.
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Background: In our hands, in vivo segmental vessel length changes up to 5% because of blood pressure: increasing in arterial pressure is associated to decrease in segmental vessel length. Methods and Material: Using two piezoelectric crystals sutured on vessel wall and a high fidelity pressure probe, we recorded artery length variations as function of blood pressure, before and after an end-to-end anastomosis on four pigs carotid arteries. Results: Mean arterial pressure before anastomosis = 73 mmHg (+/- 12); mean arterial pressure after anastomosis = 91 mmHg (+/- 14); mean crystals displacement before anastomosis during systole = -0.21mm; mean crystals displacement after anastomosis during systole = +0.24 mm; mean distance between crystals before anastomosis = 12.3 mm (+/- 0.8) and after anastomosis = 11.2 mm (+/- 0.5). Conclusions: In the acute phase following an end-to-end anastomosis, an increase in blood pressure causes increasing in vessel length, with an exponential correlation. The anastomosis is constantly subjected to a longitudinal traction whose magnitude depends on blood pressure.
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London, Gerard M. "Arterial Stiffness in Chronic Kidney Disease and End-Stage Renal Disease." Blood Purification 45, no. 1-3 (2018): 154–58. http://dx.doi.org/10.1159/000485146.
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Accelerated ageing is observed in patients with chronic kidney disease (CKD)/end-stage renal disease. Premature vascular aging and arterial stiffening are the most characteristic features of this “progeria” that is already observed in those with the early stages of CKD. Aortic stiffening is associated with high characteristic impedance, left ventricular hypertrophy, decreased coronary perfusion, and is a strong prognostic marker of mortality and cardiovascular morbidity. With aging, the arterial stiffening is more pronounced in the aorta and central arteries than in peripheral conduit arteries. This leads to progressive decrease and inversion of the arterial stiffness gradient and systemic reflection coefficient, leading to less protection of the microcirculation in the event of high-pressure transmission towards it Arterial stiffening is multifactorial with systemic microinflammation being one of the most important associated factors primarily associated with vascular calcifications.
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Osol, George, Johan Fredrik Brekke, Keara McElroy-Yaggy, and Natalia I. Gokina. "Myogenic tone, reactivity, and forced dilatation: a three-phase model of in vitro arterial myogenic behavior." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 6 (December 1, 2002): H2260—H2267. http://dx.doi.org/10.1152/ajpheart.00634.2002.
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Myogenic behavior, prevalent in resistance arteries and arterioles, involves arterial constriction in response to intravascular pressure. This process is often studied in vitro by using cannulated, pressurized arterial segments from different regional circulations. We propose a comprehensive model for myogenicity that consists of three interrelated but dissociable phases: 1) the initial development of myogenic tone (MT), 2) myogenic reactivity to subsequent changes in pressure (MR), and 3) forced dilatation at high transmural pressures (FD). The three phases span the physiological range of transmural pressures (e.g., MT, 40–60 mmHg; MR, 60–140 mmHg; FD, >140 mmHg in cerebral arteries) and are characterized by distinct changes in cytosolic calcium ([Ca2+]i), which do not parallel arterial diameter or wall tension, and therefore suggest the existence of additional regulatory mechanisms. Specifically, the development of MT is accompanied by a substantial (200%) elevation in [Ca2+]i and a reduction in lumen diameter and wall tension, whereas MR is associated with relatively small [Ca2+]i increments (<20% over the entire pressure range) despite considerable increases in wall tension and force production but little or no change in diameter. FD is characterized by a significant additional elevation in [Ca2+]i (>50%), complete loss of force production, and a rapid increase in wall tension. The utility of this model is that it provides a framework for comparing myogenic behavior of vessels of different size and anatomic origin and for investigating the underlying cellular mechanisms that govern vascular smooth muscle mechanotransduction and contribute to the regulation of peripheral resistance.
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Vrselja, Zvonimir, Hrvoje Brkic, Stefan Mrdenovic, Radivoje Radic, and Goran Curic. "Function of Circle of Willis." Journal of Cerebral Blood Flow & Metabolism 34, no. 4 (January 29, 2014): 578–84. http://dx.doi.org/10.1038/jcbfm.2014.7.
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Nearly 400 years ago, Thomas Willis described the arterial ring at the base of the brain (the circle of Willis, CW) and recognized it as a compensatory system in the case of arterial occlusion. This theory is still accepted. We present several arguments that via negativa should discard the compensatory theory. (1) Current theory is anthropocentric; it ignores other species and their analog structures. (2) Arterial pathologies are diseases of old age, appearing after gene propagation. (3) According to the current theory, evolution has foresight. (4) Its commonness among animals indicates that it is probably a convergent evolutionary structure. (5) It was observed that communicating arteries are too small for effective blood flow, and (6) missing or hypoplastic in the majority of the population. We infer that CW, under physiologic conditions, serves as a passive pressure dissipating system; without considerable blood flow, pressure is transferred from the high to low pressure end, the latter being another arterial component of CW. Pressure gradient exists because pulse wave and blood flow arrive into the skull through different cerebral arteries asynchronously, due to arterial tree asymmetry. Therefore, CW and its communicating arteries protect cerebral artery and blood–brain barrier from hemodynamic stress.
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Catalano, Maria, Giovanni Scandale, Tao Jun, Marzio Minola, Martino Recchia, and Massimo Annoni. "Radial Artery Compliance in Patients with Peripheral Vascular Disease." Vascular Medicine 2, no. 1 (February 1997): 8–12. http://dx.doi.org/10.1177/1358863x9700200102.
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Compliance in largely central arteries of patients with peripheral vascular disease (PVD) has been reported to be reduced. However, the arterial tree is an inhomogeneous system, and there remains uncertainty about whether the peripheral arteries (e.g. the medium-sized muscular radial artery) undergo a similar change to the central arteries. The aim of this study was to investigate the radial artery elasticity in 19 patients with PVD compared with 18 normal subjects of comparable age and sex. Using a noninvasive high-resolution echo-tracking device coupled to a photoplethysmograph (Finapres system) allowing simultaneous arterial diameter and finger blood pressure monitoring, we measured the radial artery compliance by determining the diameter–pressure, compliance–pressure and distensibility–pressure curves. The results showed that the diameter of the radial artery was similar in the two groups, but that the compliance and distensibility were not further reduced in patients with PVD than in the normal controls at 100 mmHg and for a common blood pressure range. The present studies demonstrate that in patients with PVD the radial arterial compliance is not reduced, which indicates that the change in arterial elasticity is not identical. The potential mechanisms involved in this change in radial artery compliance are discussed.
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Perpetuini, David, Antonio Maria Chiarelli, Vincenzo Vinciguerra, Piergiusto Vitulli, Sergio Rinella, Daniela Cardone, Francesco Bianco, et al. "Integrated Multi-channel PPG and ECG System for Cardiovascular Risk Assessment." Proceedings 27, no. 1 (September 17, 2019): 8. http://dx.doi.org/10.3390/proceedings2019027008.
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Photoplethysmography (PPG) is a non-invasive technique that employs near infrared light to estimate periodic oscillations in blood volume within arteries caused by the pulse pressure wave. Importantly, combined Electrocardiography (ECG) and PPG can be employed to quantify arterial stiffness. The capabilities of a home-made multi-channel PPG-ECG device (7 PPG probes, 4 ECG derivations) to evaluate arterial ageing were assessed. The high numerosity of channels allowed to estimate arterial stiffness at multiple body locations, without supra-systolic cuff occlusion, providing a fast and accurate examination of cardiovascular status and potentially allowing large scale clinical screening of cardiovascular risk.
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Scharf, S. M., L. M. Graver, S. Khilnani, and K. Balaban. "Respiratory phasic effects of inspiratory loading on left ventricular hemodynamics in vagotomized dogs." Journal of Applied Physiology 73, no. 3 (September 1, 1992): 995–1003. http://dx.doi.org/10.1152/jappl.1992.73.3.995.
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Exaggerated inspiratory swings in intrathoracic pressure have been postulated to increase left ventricular (LV) afterload. These predictions are based on measurements of LV afterload by use of esophageal or lateral pleural pressure. Using direct measurements of pericardial pressure, we reexamined respiratory changes in LV afterload. In 11 anesthetized vagotomized dogs, we measured arterial pressure, LV end-systolic (ES) and end-diastolic transmural (TM) pressures, stroke volume (SV), diastolic left anterior descending blood flow (CBF-D), and coronary resistance. Dogs were studied before and while breathing against an inspiratory threshold load of -20 to -25 cmH2O compared with end expiration. Relative to end expiration, SV and LVES TM pressures decreased during inspiration and increased during early expiration, effects exaggerated during inspiratory loading. In all cases, LV afterload (LVES TM pressure) changed in parallel with SV. LV end-diastolic TM pressure did not change. CBF-D paralleled arterial pressure, and there were no changes in coronary resistance. In two dogs, regional LVES segment length paralleled calculated changes in LVES TM pressure. We conclude that 1) LV afterload decreases during early inspiration and increases during early expiration, changes secondary to those in SV; 2) changes in CBF-D are secondary to changes in perfusion pressure during the respiratory cycle; and 3) the use of esophageal or lateral pleural pressure to estimate LV surface pressure overestimates changes in LV TM pressures during respiration.
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Saito, T., I. Yamamoto, X.-L. Huang, N. Yukawa, M. Osawa, and S. Takeichi. "Effects of muscle relaxants on EEG, ABR and EMG in rabbits." Human & Experimental Toxicology 18, no. 12 (December 1999): 718–23. http://dx.doi.org/10.1191/096032799678839635.
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The effects of baclofen and pancuronium bromide on evoked electromyogram (EMG), cortical electroencephalogram (EEG) and auditory brainstem responses (ABR) were studied in pentobarbital anesthetized normal rabbits. Evoked EMG was measured in the gastrocnemius muscle by electrical stimulation of the sciatic nerve. Intravenous injection of baclofen decreased EEG and arterial blood pressure and light reflex, however, it had no significant influence on EMG or ABR at doses of 10 and 20 mg/kg/h. Pancuronium bromide immediately inhibited respiration, decreased EEG and EMG, however, it had no significant influence on arterial blood pressure, ABR, or light reflex, at doses of 0.4 and 1.0 mg/kg/h in anesthetized rabbits. ABR waves were observed until just before cardiac arrest with both of the muscle relaxants. It is suggested that ABR are not influenced by central or peripheral muscle relaxants, or by pentobarbital.
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Dobbin, K., S. Wallace, J. Ahlberg, and M. Chulay. "Pulmonary artery pressure measurement in patients with elevated pressures: effect of backrest elevation and method of measurement." American Journal of Critical Care 1, no. 2 (September 1, 1992): 61–69. http://dx.doi.org/10.4037/ajcc1992.1.2.61.
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OBJECTIVE: To determine whether pulmonary artery pressure measurement is accurate if the head of the bed is elevated; to compare the end-expiratory graphic recording and digital monitor methods for pulmonary artery pressure measurement; to determine whether either mean arterial pressure or mixed venous oxygen saturation changes during backrest elevation. DESIGN: Nonrandomized clinical trial. SETTING: A six-bed cardiac surgical intensive care unit of a 540-bed federal facility. POPULATION: Twenty-five postoperative cardiac surgical patients with elevated pulmonary artery pressures (systolic higher than 35 mm Hg). INTERVENTIONS: In supine patients pulmonary artery pressures were measured at each of the following backrest elevations: 0, 20, 30, 45 and again at 0 degrees. Measurements were obtained once during mechanical ventilation and once during normal breathing after extubation. MAIN OUTCOME MEASURES: End-expiratory graphic recording of pulmonary artery pressures; digital monitor values of pulmonary artery pressures; mean arterial pressure; and mixed venous oxygen saturation. RESULTS: No statistical difference was found in pulmonary artery pressures measured at each of the backrest elevations during mechanical ventilation or normal breathing after extubation. Pulmonary artery diastolic and pulmonary capillary wedge pressures obtained with the digital monitor method were significantly lower than the end expiratory graphic recording method during normal breathing after extubation but not during mechanical ventilation. No changes in mean arterial pressure or mixed venous oxygen saturation occurred during backrest elevation. CONCLUSIONS: These results show that pulmonary artery pressures can be measured accurately with the head of the bed in an elevated position. The data indicate that obtaining pulmonary artery pressure measurements from the digital display of the bedside monitor is accurate when respiratory wave form fluctuations are minimal but may lead to inaccurate values with prominent respiratory fluctuations. Further research is needed to validate this finding in different patient populations and with other models of monitoring equipment.
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Zhang, Yi, Patrick Lacolley, Athanase D. Protogerou, and Michel E. Safar. "Arterial Stiffness in Hypertension and Function of Large Arteries." American Journal of Hypertension 33, no. 4 (February 15, 2020): 291–96. http://dx.doi.org/10.1093/ajh/hpz193.
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Abstract BACKGROUND Arterial stiffness—typically assessed from non-invasive measurement of pulse wave velocity along a straight portion of the vascular tree between the right common carotid and femoral arteries—is a reliable predictor of cardiovascular risk in patients with essential hypertension. METHODS We reviewed how carotid-femoral pulse wave velocity increases with age and is significantly higher in hypertension (than in age- and gender-matched individuals without hypertension), particularly when hypertension is associated with diabetes mellitus. RESULTS From the elastic aorta to the muscular peripheral arteries of young healthy individuals, there is a gradual but significant increase in stiffness, with a specific gradient. This moderates the transmission of pulsatile pressure towards the periphery, thus protecting the microcirculatory network. The heterogeneity of stiffness between the elastic and muscular arteries causes the gradient to disappear or be inversed with aging, particularly in long-standing hypertension. CONCLUSIONS In hypertension therefore, pulsatile pressure transmission to the microcirculation is augmented, increasing the potential risk of damage to the brain, the heart, and the kidney. Furthermore, elevated pulse pressure exacerbates end-stage renal disease, particularly in older hypertensive individuals. With increasing age, the elastin content of vessel walls declines throughout the arterial network, and arterial stiffening increases further due to the presence of rigid wall material such as collagen, but also fibronectin, proteoglycans, and vascular calcification. Certain genes, mainly related to angiotensin and/or aldosterone, affect this aging process and contribute to the extent of arterial stiffness, which can independently affect both forward and reflected pressure waves.
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Cooke, William H., Jason R. Carter, and Tom A. Kuusela. "Human cerebrovascular and autonomic rhythms during vestibular activation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 286, no. 5 (May 2004): R838—R843. http://dx.doi.org/10.1152/ajpregu.00562.2003.
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Otolith activation increases muscle sympathetic nerve activity (MSNA), and MSNA activation may alter associations among autonomic oscillators, including those modulating cerebral hemodynamics. The purpose of this study was to determine the influence of vestibulosympathetic activation on cerebral and autonomic rhythms. We recorded the ECG, finger arterial pressure, end-tidal CO2, respiration, cerebral blood flow velocity, and MSNA in eight subjects. Subjects breathed at 0.25 Hz for 5 min in the prone and head-down positions. We analyzed data in time and frequency domains and performed cross-spectral analyses to determine coherence and transfer function magnitude. Head-down rotation increased MSNA from 7 ± 1.3 to 12 ± 1.5 bursts/min ( P = 0.001) but did not affect R-R intervals, arterial pressures, mean cerebral blood flow velocities ( Vmean), or their power spectra. Vestibular activation with head-down rotation had no effect on mean arterial pressure and Vmean transfer function magnitude. The two new findings from this study are 1) head-down rotation independently activates the sympathetic nervous system with no effect on parasympathetic activity or Vmean; and 2) frequency-dependent associations between arterial pressures and Vmean are independent of vestibular activation. These findings support the concept that vestibular-autonomic interactions independently and redundantly serve to maintain steady-state hemodynamics.
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Peng, Ying-I., and Kuo-Chu Chang. "Acute effects of methoxamine on left ventricular-arterial coupling in streptozotocin-diabetic rats: a pressure-volume analysis." Canadian Journal of Physiology and Pharmacology 78, no. 5 (April 10, 2000): 415–22. http://dx.doi.org/10.1139/y00-005.
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We determined the acute effects of methoxamine, a specific alpha1-selective adrenoceptor agonist, on the left ventricular-arterial coupling in streptozotocin (STZ)-diabetic rats, using the end-systolic pressure-stroke volume relationships. Rats given STZ 65 mg·kg-1 iv (n = 8) were compared with untreated age-matched controls (n = 8). A high-fidelity pressure sensor and an electromagnetic flow probe measured left ventricular (LV) pressure and ascending aortic flow, respectively. Both LV end-systolic elastance ELV,ES and effective arterial elastance Ea were estimated from the pressure-ejected volume loop. The optimal afterload Qload determined by the ratio of Ea to ELV,ES was used to measure the optimality of energy transmission from the left ventricle to the arterial system. In comparison with controls, diabetic rats had decreased LV end-systolic elastance ELV,ES, at 513 ± 30 vs. 613 ± 29 mmHg·mL-1, decreased effective arterial elastance Ea, at 296 ± 20 vs. 572 ± 48 mmHg·mL-1, and decreased optimal afterload Qload, at 0.938 ± 0.007 vs. 0.985 ± 0.009. Methoxamine administration to STZ-diabetic rats significantly increased LV end-systolic elastance ELV,ES, from 513 ± 30 to 602 ± 38 mmHg·mL-1, and effective arterial elastance Ea, from 296 ± 20 to 371 ± 28 mmHg·mL-1, but did not change optimal afterload Qload. We conclude that diabetes worsens not only the contractile function of the left ventricle, but also the matching condition for the left ventricular-arterial coupling. In STZ-diabetic rats, administration of methoxamine improves the contractile status of the ventricle and arteries, but not the optimality of energy transmission from the left ventricle to the arterial system. Key words: streptozotocin-diabetic rats, left ventricular-arterial coupling, left ventricular end-systolic elastance, effective arterial elastance, optimal afterload.
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Srinivas, Arun, Madathil Ranjit, James L. Wilkinson, Tiow Goh, Brian Edis, Samuel Menahem, Lance Fong, and Robert Weintraub. "Hemodynamic and angiographic findings following arterial switch repair for complete transposition." Cardiology in the Young 6, no. 4 (October 1996): 298–307. http://dx.doi.org/10.1017/s1047951100003929.
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AbstractThe arterial switch operation is the treatment of choice for complete transposition, and for the Taussig-Bing anomaly, with good early and mid-term results. This retrospective study examined the findings obtained at routine follow-up cardiac catheterization after primary arterial switch repair. We catheterized 111 patients after a mean of 16.9 months after surgery. These included 67 patients with an intact ventricular septum, 33 with a ventricular septal defect, and 11 with the Taussig-Bing anomaly. Right ventricular pressures were mildly elevated (mean 33.9±10.2 mm Hg) in the overall group with a mean pressure ratio between right and left ventricles of 0.34±0.1. Of the patients 74% had gradients across the right ventricular outflow tract of under 20 mm Hg, while three (2.7%) had gradients over 30 mm Hg. A significant gradient across the left ventricular outflow tract occurred in one patient (0.9%), while significant neo-aortic stenosis was not seen. The neo-aortic root remained dilated, with mild aortic valvar incompetence being seen in 12%, with none having higher grades of regurgitation. Left ventricular ejection fraction was normal in all patients, while left ventricular end-diastolic pressure was elevated in 38%. Coronary arterial stenosis was not seen, but one patient (0.9%) had left ventricular apical dyskinesia. Overall, therefore, we conclude that cardiac hemodynamics and ventricular systolic function after primary arterial switch are good. Minor gradients to the pulmonary arteries, and mild neo-aortic valvar incompetence were commonly noted. Left ventricular end-diastolic pressure was elevated in over a third of the patients. These subclinical and subtle abnormalities warrant ongoing follow-up to determine their long-term significance.
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Henning, R. J. "Effects of positive end-expiratory pressure on the right ventricle." Journal of Applied Physiology 61, no. 3 (September 1, 1986): 819–26. http://dx.doi.org/10.1152/jappl.1986.61.3.819.
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Transmural cardiac pressures, stroke volume, right ventricular volume, and lung water content were measured in normal dogs and in dogs with oleic acid-induced pulmonary edema (PE) maintained on positive-pressure ventilation. Measurements were performed prior to and following application of 20 cmH2O positive end-expiratory pressure (PEEP). Colloid fluid was given during PEEP for ventricular volume expansion before and after the oleic acid administration. PEEP significantly increased pleural pressure and pulmonary vascular resistance but decreased right ventricular volume, stroke volume, and mean arterial pressure in both normal and PE dogs. Although the fluid infusion during PEEP raised right ventricular diastolic volumes to the pre-PEEP level, the stroke volumes did not significantly increase in either normal dogs or the PE dogs. The fluid infusion, however, significantly increased the lung water content in the PE dogs. Following discontinuation of PEEP, mean arterial pressure, cardiac output, and stroke volume significantly increased, and heart rate did not change. The failure of the stroke volume to increase despite significant right ventricular volume augmentation during PEEP indicates that positive-pressure ventilation with 20 cmH2O PEEP decreases right ventricular function.
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Zárate Méndez, Luis Hernán, and Alex Valenzuela Montero. "Sodium-potassium balance in the regulation of high blood pressure." Medwave 12, no. 02 (February 1, 2012): e5301-e5301. http://dx.doi.org/10.5867/medwave.2012.02.5301.
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Davies, R. J., P. J. Belt, S. J. Roberts, N. J. Ali, and J. R. Stradling. "Arterial blood pressure responses to graded transient arousal from sleep in normal humans." Journal of Applied Physiology 74, no. 3 (March 1, 1993): 1123–30. http://dx.doi.org/10.1152/jappl.1993.74.3.1123.
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During obstructive sleep apnea, transient arousal at the resumption of breathing is coincident with a substantial rise in blood pressure. To assess the hemodynamic effect of arousal alone, 149 transient stimuli were administered to five normal subjects. Two electroencephalograms (EEG), an electrooculogram, a submental electromyogram (EMG), and beat-to-beat blood pressure (Finapres, Ohmeda) were recorded in all subjects. Stimulus length was varied to produce a range of cortical EEG arousals that were graded as follows: 0, no increase in high-frequency EEG or EMG; 1, increased high-frequency EEG and/or EMG for < 10 s; 2, increased high-frequency EEG and/or EMG for > 10 s. Overall, compared with control values, average systolic pressure rose [nonrapid-eye-movement (NREM) sleep 10.0 +/- 7.69 (SD) mmHg; rapid-eye-movement (REM) sleep 6.0 +/- 6.73 mmHg] and average diastolic pressure rose (NREM sleep 6.1 +/- 4.43 mmHg; REM sleep 3.7 +/- 3.02 mmHg) over the 10 s following the stimulus (NREM sleep, P < 0.0001; REM sleep, P < 0.002). During NREM sleep, there was a trend toward larger blood pressure rises at larger grades of arousal (systolic: r = 0.22, 95% confidence interval 0.02–0.40; diastolic: r = 0.48, 95% confidence interval 0.31–0.62). The average blood pressure rise in response to the grade 2 arousals was approximately 75% of that during obstructive sleep apnea. Arousal stimuli that did not cause EEG arousal still produced a blood pressure rise (mean systolic rise 8.6 +/- 7.0 mmHg, P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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Chemla, D., J. L. Hebert, C. Coirault, S. Salmeron, K. Zamani, and Y. Lecarpentier. "Matching dicrotic notch and mean pulmonary artery pressures: implications for effective arterial elastance." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 4 (October 1, 1996): H1287—H1295. http://dx.doi.org/10.1152/ajpheart.1996.271.4.h1287.
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It has been suggested that pulmonary artery pressure at the end of ejection is close to mean pulmonary artery pressure, thus contributing to the optimization of external power from the right ventricle. We tested the hypothesis that dicrotic notch and mean pulmonary artery pressures could be of similar magnitude in 15 men (50 +/- 12 yr) referred to our laboratory for diagnostic right and left heart catheterization. Beat-to-beat relationships between dicrotic notch and mean pulmonary artery pressures were studied 1) at rest over 10 consecutive beats and 2) in 5 patients during the Valsalva maneuver (178 beats studied). At rest, there was no difference between dicrotic notch and mean pulmonary artery pressures (21.8 +/- 12.0 vs. 21.9 +/- 11.1 mmHg). There was a strong linear relationship between dicrotic notch and mean pressures 1) over the 10 consecutive beats studied in each patient (mean r = 0.93), 2) over the 150 resting beats (r = 0.99), and 3) during the Valsalva maneuver in each patient (r = 0.98-0.99) and in the overall beats (r = 0.99). The difference between dicrotic notch and mean pressures was -0.1 +/- 1.7 mmHg at rest and -1.5 +/- 2.3 mmHg during the Valsalva maneuver. Substitution of the mean pulmonary artery pressure by the dicrotic notch pressure in the standard formula of the pulmonary vascular resistance (PVR) resulted in an equation relating linearly end-systolic pressure and stroke volume. The slope of this relation had the dimension of a volume elastance (in mmHg/ml), a simple estimate of volume elastance being obtained as 1.06(PVR/T), where T is duration of the cardiac cycle. In conclusion, dicrotic notch pressure was of similar magnitude as mean pulmonary artery pressure. These results confirmed our primary hypothesis and indicated that human pulmonary artery can be treated as if it is an elastic chamber with a volume elastance of 1.06(PVR/T).
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Cates, Matthew J., Peter W. Steed, Ana P. L. Abdala, Philip D. Langton, and Julian F. R. Paton. "Elevated vertebrobasilar artery resistance in neonatal spontaneously hypertensive rats." Journal of Applied Physiology 111, no. 1 (July 2011): 149–56. http://dx.doi.org/10.1152/japplphysiol.00220.2011.
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There is a strong correlation between increased vertebral artery resistance and arterial blood pressure in humans. The reasons for this increased resistance at high systemic pressure remain unknown, but may include raised sympathetic activity. With the recent finding that prehypertensive spontaneously hypertensive (PHSH) rats, which have raised sympathetic nerve activity, but a blood pressure comparable to normotensive rat strains, we hypothesized that its vertebrobasilar vascular resistance would already be raised and, as a consequence, would exhibit a more responsive Cushing response (e.g., brain ischemia evoked sympathoexcitation and a pressor response). We report that PHSH rats exhibited a remodeling of the basilar artery (i.e., increased wall thickness and lower lumen-to-wall thickness ratio) that occurred before the onset of hypertension. In a novel in vitro vascularly isolated, arterially perfused brain stem preparation of PHSH rats of 4–5 wk of age, brain stem vascular resistance was raised by ∼35% relative to age- and sex-matched normotensive rats ( P < 0.05). In the in situ arterial perfused working heart-brain stem preparation, occlusion of both vertebral arteries in the PHSH rat resulted in a significantly greater increase in sympathetic activity (57 vs. 20%, PHSH vs. control; P < 0.01) that triggered a greater increase in arterial perfusion pressure (8 vs. 3 mmHg, PHSH vs. control; P < 0.01) compared with normotensive rats. These data indicate raised vertebrobasilar artery resistance before the onset of hypertension in the PHSH rat. With the raised responsiveness of the Cushing response in the PHSH rat, we discuss the possibility of brain stem perfusion as a central nervous system determinant of the set point of vasomotor sympathetic tone in the hypertensive condition.
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Sugawara, Jun, Tsubasa Tomoto, Hsin-Fu Lin, Chen-Huan Chen, and Hirofumi Tanaka. "Aortic reservoir function of Japanese female pearl divers." Journal of Applied Physiology 125, no. 6 (December 1, 2018): 1901–5. http://dx.doi.org/10.1152/japplphysiol.00466.2018.
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Female pearl divers in Japan, called “ Ama,” engage in repeated breath-hold free-diving maneuvers for collecting pearls, seaweeds, and shellfish in the cold sea. We previously reported that they have lower systemic arterial stiffness than age-matched sedentary peers. As a follow-up study, we evaluated their segmental arterial stiffness and aortic reservoir function. A total of 120 non-medicated women living in the same fishing villages (mean age: 65 ± 11 yr), including 88 Ama and 32 age-matched sedentary peers, were studied. Pulse wave velocity from the heart to the brachial artery (hbPWV; partly reflecting proximal aortic stiffness) and between the brachial artery and the ankle (baPWV; reflecting stiffness of abdominal aorta and leg arteries) were measured. Aortic hemodynamic variables were estimated from applanation tonometry carotid arterial pressure waveforms via general transfer function. Carotid artery impedance was calculated from blood flow velocity and blood pressure of contralateral common carotid arteries. baPWV was not different between the groups ( P = 0.117), whereas hbPWV was significantly lower in pearl divers than sedentary peers ( P = 0.004). Additionally, Ama had significantly lower aortic reservoir pressure integral ( P = 0.029) and carotid artery impedance modulus in frequency ranges from 0.78 to 4.0 Hz ( P = 0.011~0.019) than in sedentary peers. Collectively, these findings indicate that lifelong female pearl divers have superior reservoir function in central elastic arteries (e.g., the proximal aorta and carotid artery) in comparison with age-matched sedentary women living in the same fishing village. NEW & NOTEWORTHY We previously reported that lifelong female pearl divers in Japan, called “ Ama,” have lower systemic arterial stiffness than age-matched sedentary peers. As a follow-up study, we evaluated their segmental arterial stiffness and aortic reservoir function. In comparison with age-matched sedentary women living in the same fishing village, Ama demonstrated significantly lower arterial stiffness in more proximal and elastic arterial segments and superior reservoir function in central elastic arteries.
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Umapathy, E., S. T. Muthiraparampil, and A. Namugowa. "Assessment of variations in arterial tone during different phases of menstrual cycle." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 8, no. 5 (April 29, 2019): 1810. http://dx.doi.org/10.18203/2320-1770.ijrcog20191924.
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Background: Arterial tone parameters in young African women during the different phases of menstrual cycle were assessed in the present study.Methods: Out of the 30 student volunteers who participated in the study, only 15 completed the study. Anthropometric data using stadiometer, blood pressure using automated oscillometric pressure gauge were measured. Arterial stiffness parameters at the radial and ECG gated carotid and femoral arteries using sphygmocor tonometry was mesured in two consecutive menstrual cycles at early follicular, ovulation and luteal phase. Estrogen and progesterone concentrations were analyzed using Elisa kits in all three phases.Results: Estrogen level in ovulation phase and progesterone in luteal phase were higher. Peripheral augmentation index in ovulation phase was higher compared to luteal phase. Pulse pressure amplification value at follicular and luteal phases was higher than in ovulation phase. Pulse wave velocity and pulse pressure amplification was negatively correlated to progesterone in follicular phase. The arterial stiffness increased at ovulation and decreased in follicular and luteal phases of menstrual cycle.Conclusions: No significant correlation between arterial stiffness parameters and ovarian hormones was found.
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Markstrom, Agneta M., Michael Lichtwarck-Aschoff, Bjorn A. Svensson, K. Anders Nordgren, and Ulf H. Sjostrand. "Ventilation with Constant Versus Decelerating Inspiratory Flow in Experimentally Induced Acute Respiratory Failure." Anesthesiology 84, no. 4 (April 1, 1996): 882–89. http://dx.doi.org/10.1097/00000542-199604000-00016.
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Background Recognition of the potential for ventilator-associated lung injury has renewed the debate on the importance of the inspiratory flow pattern. The aim of this study was to determine whether a ventilatory pattern with decelerating inspiratory flow, with the major part of the tidal volume delivered early, would increase functional residual capacity at unchanged (or even reduced) inspiratory airway pressures and improve gas exchange at different positive end-expiratory pressure levels. Methods Surfactant depletion was induced by repeated bronchoalveolar lavage in 13 anesthetized piglets. Decelerating and constant inspiratory flow ventilation was applied at positive end-expiratory pressure levels of 22, 17, 13, 9, and 4 cm H(2)O. Tidal volume, inspiration-to-expiration ratio, and ventilatory frequency were kept constant. Airway pressures, gas exchange, functional residual capacity (using a wash-in/washout method with sulfurhexafluoride), central hemodynamics, and extravascular lung water (using the thermo-dye-indicator dilution technique) were measured. Results Decelerating inspiratory flow yielded a lower arterial carbon dioxide tension compared to constant flow, that is, it improved alveolar ventilation. There were no differences between the flow patterns regarding end-inspiratory occlusion airway pressure, end-inspiratory lung volume, static compliance, or arterial oxygen tension. No differences were seen in hemodynamics and oxygen delivery. Conclusions The decelerating inspiratory flow pattern increased carbon dioxide elimination, without any reduction of inspiratory airway pressure or apparent improvement in arterial oxygen tension. It remains to be established whether these differences are sufficiently pronounced to justify therapeutic consideration.
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Maron, M. B. "A canine model of neurogenic pulmonary edema." Journal of Applied Physiology 59, no. 3 (September 1, 1985): 1019–25. http://dx.doi.org/10.1152/jappl.1985.59.3.1019.
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The purpose of this study was to evaluate the usefulness of the intracisternal administration of veratrine as a model of neurogenic pulmonary edema (NPE) in the alpha-chloralose-anesthetized dog. Veratrine (40–60 micrograms/kg) was injected into the cisterna magna of 17 animals, and systemic arterial, pulmonary arterial, and left ventricular end-diastolic (LVEDP) pressures were followed for 1 h. Eleven animals developed alveolar edema. In these animals, systemic arterial pressure increased to 273 +/- 9 (SE) Torr, pulmonary arterial pressure to 74.5 +/- 4.9 Torr, and LVEDP to 42.8 +/- 4.5 Torr, and large amounts of pink frothy fluid, with protein concentrations ranging from 48 to 93% of plasma, appeared in the airways. Postmortem extravascular lung water content (Qwl/dQl) averaged 7.30 +/- 0.46 g H2O/g dry lung wt. Six animals escaped developing this massive degree of edema after veratrine (Qwl/dQl = 4.45 +/- 0.24). These animals exhibited similar elevated systemic arterial pressures (268 +/- 15 Torr), but did not develop the degree of pulmonary hypertension (pulmonary arterial pressure = 52.5 +/- 6.7 Torr, LVEDP = 24.8 +/- 4.0 Torr) observed in the other group. These results suggest that both hemodynamic and permeability mechanisms may play a role in the development of this form of edema and that veratrine administration may provide a useful model of NPE.
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Agarwal, Rajiv. "Relationship between circadian blood pressure variation and circadian protein excretion in CKD." American Journal of Physiology-Renal Physiology 293, no. 3 (September 2007): F655—F659. http://dx.doi.org/10.1152/ajprenal.00188.2007.
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Circadian blood pressure changes are blunted in patients with chronic kidney disease (CKD). Proteinuria is the most important correlate of hypertension in CKD. However, little is known about the influence of circadian blood pressure changes and variation in protein excretion rate. Furthermore, the impact of blood pressure components, e.g., mean arterial pressure and pulse pressure, on proteinuria has not been evaluated. To analyze the relationship of circadian changes in blood pressure on urinary protein excretion patterns, glomerular filtration rate was measured with iothalamate clearance and 24-h ambulatory blood pressure with SpaceLabs 90207 monitor in 22 patients with CKD. It was found that hourly protein excretion rates were 31% higher during the night. Excretion results of sodium, potassium, chloride, urea, and creatinine were also between 30 and 40% higher at night. Systolic, mean arterial, and pulse pressures but not diastolic pressure were related to daytime protein excretion rate. At night, the relationship of systolic, diastolic, and mean arterial pressures was significantly lower and essentially flat with respect to protein excretion rate, but the relationship of pulse pressure and proteinuria was not different from that seen during the day. Circadian variation in blood pressure did not impact circadian sodium excretion rate. In conclusion, these data suggest that patients with CKD have patterns of proteinuria that share different relationships with blood pressure components depending on the awake-sleep state. Pulse pressure is related to proteinuria independent of the awake-sleep state. Reducing mean arterial pressure during the day and pulse pressure during the day or night may be effective antiproteinuric strategies.
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Reddy, Yogesh N. V., Abdallah El-Sabbagh, and Rick A. Nishimura. "Comparing Pulmonary Arterial Wedge Pressure and Left Ventricular End Diastolic Pressure for Assessment of Left-Sided Filling Pressures." JAMA Cardiology 3, no. 6 (June 1, 2018): 453. http://dx.doi.org/10.1001/jamacardio.2018.0318.
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Ouyang, An, T. Dylan Olver, Craig A. Emter, and Bradley S. Fleenor. "Chronic exercise training prevents coronary artery stiffening in aortic-banded miniswine: role of perivascular adipose-derived advanced glycation end products." Journal of Applied Physiology 127, no. 3 (September 1, 2019): 816–27. http://dx.doi.org/10.1152/japplphysiol.00146.2019.
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Heart failure (HF) is associated with increased large conduit artery stiffness and afterload resulting in stiffening of the coronary arteries. Perivascular adipose tissue (PVAT) and advanced glycation end products (AGE) both promote arterial stiffness, yet the mechanisms by which coronary PVAT promotes arterial stiffness and the efficacy of exercise to prevent coronary stiffness are unknown. We hypothesized that both chronic continuous and interval exercise training would prevent coronary PVAT-mediated AGE secretion and arterial stiffness. Yucatan miniature swine were divided into four groups: control-sedentary (CON), aortic banded sedentary-heart failure (HF), aortic banded HF-continuous exercise trained (HF+CONT), and aortic banded HF-interval exercise trained (HF+IT). The left circumflex and right coronary arteries underwent ex vivo mechanical testing, and arterial AGE, elastin, and collagen were assessed. Coronary elastin elastic modulus (EEM) and elastin protein were lower and AGE was increased with HF compared with CON, which was prevented by both HF+CONT and HF+IT. Mouse aortic segments treated with swine coronary PVAT conditioned medium had lower EEM and elastin content and greater AGE secretion and arterial AGE accumulation in HF compared with CON, which was prevented by both HF+CONT and HF+IT. Aminoguanidine (AMG), an AGE inhibitor, prevented the reduction in EEM, arterial elastin content, and AGE accumulation in mouse aortic segments treated with PVAT conditioned medium in the HF group. Our data demonstrate efficacy for chronic continuous and interval exercise to prevent coronary artery stiffness via inhibition of PVAT-derived AGE secretion in a preclinical miniswine model of pressure overload-induced HF. NEW & NOTEWORTHY Our findings show that chronic continuous and interval exercise training regimens prevent coronary artery stiffness associated with inhibition of perivascular adipose tissue-derived advanced glycation end products in a translational pressure overload-induced heart failure model potentially providing an effective therapeutic option for heart failure patients.
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Conrad, Kirk P., Dan O. Debrah, Jackie Novak, Lee A. Danielson, and Sanjeev G. Shroff. "Relaxin Modifies Systemic Arterial Resistance and Compliance in Conscious, Nonpregnant Rats." Endocrinology 145, no. 7 (July 1, 2004): 3289–96. http://dx.doi.org/10.1210/en.2003-1612.
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Abstract Relaxin emanates from the corpus luteum of the ovary and circulates during pregnancy. Because the hormone is a potent renal vasodilator and mediates the renal vasodilation and hyperfiltration of pregnancy in conscious rats, we reasoned that it might also contribute to the broader cardiovascular changes of pregnancy. We began investigating this concept by testing whether relaxin can modify systemic arterial hemodynamics and load when chronically administered to nonpregnant rats. The major objectives of the present work were to determine whether relaxin administration to nonpregnant rats 1) modifies cardiac output (CO), systemic vascular resistance, and global arterial compliance (AC), and 2) regulates the passive mechanics of isolated arteries. To accomplish the first objective, we developed a conscious rat model for assessment of global AC. Passive mechanics of small renal arteries were assessed using a pressure arteriograph. Chronic administration of recombinant human relaxin by sc osmotic minipump to conscious, female, nonpregnant rats reduced the steady arterial load by decreasing systemic vascular resistance, increased CO, and reduced the pulsatile arterial load by increasing global AC as quantified by two indices—AC estimated from the diastolic decay of aortic pressure and CO and AC estimated by the ratio of stroke volume-to-pulse pressure. In another group of rats, relaxin administration also regulated the passive mechanics of small renal arteries, indicating that, in addition to reduction in vascular smooth muscle tone, modification of the vascular structure (e.g. extracellular matrix) contributes to the increase in global AC. These findings suggest a role for relaxin in the systemic hemodynamic changes of pregnancy, as well as novel therapeutic potential for relaxin in modifying arterial stiffness and cardiac afterload.
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Takeuchi, Muneyuki, Sven Goddon, Marisa Dolhnikoff, Motomu Shimaoka, Dean Hess, Marcelo B. P. Amato, and Robert M. Kacmarek. "Set Positive End-expiratory Pressure during Protective Ventilation Affects Lung Injury." Anesthesiology 97, no. 3 (September 1, 2002): 682–92. http://dx.doi.org/10.1097/00000542-200209000-00023.
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Background The most appropriate method of determining positive end-expiratory pressure (PEEP) level during a lung protective ventilatory strategy has not been established. Methods In a lavage-injured sheep acute respiratory distress syndrome model, the authors compared the effects of three approaches to determining PEEP level after a recruitment maneuver: (1) 2 cm H(2)O above the lower inflection point on the inflation pressure-volume curve, (2) at the point of maximum curvature on the deflation pressure-volume curve, and (3) at the PEEP level that maintained target arterial oxygen partial pressure at a fraction of inspired oxygen of 0.5. Results Positive end-expiratory pressure set 2 cm H(2)O above the lower inflection point resulted in the least injury over the course of the study. PEEP based on adequate arterial oxygen partial pressure/fraction of inspired oxygen ratios had to be increased over time and resulted in higher mRNA levels for interleukin-8 and interleukin-1beta and greater tissue inflammation when compared with the other approaches. PEEP at the point of maximum curvature could not maintain eucapneia even at an increased ventilatory rate. Conclusion Although generating higher plateau pressures, PEEP levels based on pressure-volume curve analysis were more effective in maintaining gas exchange and minimizing injury than PEEP based on adequate oxygenation. PEEP at 2 cm H(2)O above the lower inflection point was most effective.
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Repessé, Xavier, Cyril Charron, Guillaume Geri, Alix Aubry, Alexis Paternot, Julien Maizel, Michel Slama, and Antoine Vieillard-Baron. "Impact of positive pressure ventilation on mean systemic filling pressure in critically ill patients after death." Journal of Applied Physiology 122, no. 6 (June 1, 2017): 1373–78. http://dx.doi.org/10.1152/japplphysiol.00958.2016.
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Mean systemic filling pressure (Pms) defines the pressure measured in the venous-arterial system when the cardiac output is nil. Its estimation has been proposed in patients with beating hearts by building the venous return curve, using different pairs of right atrial pressure/cardiac output during mechanical ventilation. We raised the hypothesis according to which the Pms is altered by tidal ventilation and positive end-expiratory pressure (PEEP), which would challenge this extrapolation method based on cardiopulmonary interactions. We conducted a two-center, noninterventional, observational, and prospective study, using an arterial and a venous catheter to measure the pressure in the circulatory system at the time of death in critically ill, mechanically ventilated patients with a PEEP. Arterial (Part) and venous pressures (Pra) were recorded in five conditions: at end expiration and end inspiration with and without PEEP and finally once the ventilator was disconnected. Part and Pra did not differ in any experimental conditions. Tidal ventilation increased Pra and Part by 2.4 and 1.9 mmHg, respectively, whereas PEEP increased both values by 1.2 and 1 mmHg, respectively. After disconnection of the ventilator, Pra and Part were 10.0 ± 4.2 and 9.9 ± 4.2 mmHg, respectively. Pms increases during mechanical ventilation, with an effect of tidal ventilation and PEEP. This calls into question the validity of its evaluation in heart-beating patients using cardiopulmonary interactions during mechanical ventilation. NEW & NOTEWORTHY The physiology of the mean systemic filling pressure (Pms) is not well understood in human beings. This study is the first report of a tidal ventilation- and positive end-expiratory pressure-related increase in Pms in critically ill patients. The results challenge the utility and the value estimating Pms in heart-beating patients by reconstruction of the venous return curve using varying inflation pressures.
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Saito, O., W. J. Lamm, J. Hildebrandt, and R. K. Albert. "Flow pulsatility does not increase mean microvascular pressure or filtration in zone 3 rabbit lungs." Journal of Applied Physiology 78, no. 3 (March 1, 1995): 914–20. http://dx.doi.org/10.1152/jappl.1995.78.3.914.
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We previously reported that mean pulmonary arterial pressure (Ppa) during pulsatile flow exceeded that for steady flow when flow was greater than the normal resting value and speculated that this was due to irregularities of the flow profiles in precapillary vessels, mainly the larger arteries. From this we hypothesized that neither mean microvascular pressure nor the rate of fluid filtration would be affected by flow pulsatility. We therefore compared the effects of steady vs. pulsatile flow on the double-occlusion pressure (Pdo) and on edema formation (rate of weight gain) in zone 3 rabbit lungs. Excised left lungs (n = 19) were perfused with Tyrode solution and ventilated with an end-expiratory pressure of 2.5 cmH2O. A diaphragm pump generated pulsatile flow with a stroke volume of 1.0 ml (approximately 0.8 the normal resting value for rabbit left lung). Nonpulsatile flow was generated by raising an arterial reservoir. Flow rate was set at 100 or 400 ml/min (approximately 0.4 or 1.6 x the normal resting cardiac output, respectively). Vascular pressures (referenced to the bottom of the lung) were measured after ventilation, at end expiration, was interrupted. Pdo values were obtained in random order at 15 time points that were evenly distributed within the pulse cycle, averaged across pulses to obtain the mean capillary pressure profile, and then averaged over time. At the lower flow of 100 ml/min, mean Ppa and Pdo were slightly lower (3–4%) during pulsatile compared with nonpulsatile conditions. At the higher flow of 400 ml/min, mean Ppa was higher under pulsatile conditions (13%), whereas downstream the mean Pdo values were equal.(ABSTRACT TRUNCATED AT 250 WORDS)
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Marjanovic, Ivan, Antonio Martinez, Marija Marjanovic, Djordje Kontic, Paraskeva Hentova-Sencanic, Vujica Markovic, and Marija Bozic. "Changes in the retrobulbar arterial circulation after decrease of the elevated intraocular pressure in men and women with primary open angle glaucoma." Srpski arhiv za celokupno lekarstvo 141, no. 11-12 (2013): 728–31. http://dx.doi.org/10.2298/sarh1312728m.
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Introduction. An altered perfusion of the optic nerve head has been proposed as a pathogenic factor of glaucoma. Objective. The aim of this study was to evaluate the changes of the hemodynamic parameters in the retrobulbar arterial circulation after decrease of the elevated intraocular pressure (IOP) in women and men with primary open angle glaucoma. Methods. The study included 60 patients (33 males and 27 females) older than 50 years, with diagnosed and treated primary open angle glaucoma (77 eyes of 39 patients had increased IOP, >25 mm Hg). They were examined at the Clinic of Eye Diseases (complete ophthalmologic exam) and Clinic of Neurology, Clinical Center of Serbia, Belgrade, from December 2009 to December 2010. Imaging of hemodynamic parameters of three retrobulbar arterial vessels: ophthalmic, central retinal and posterior ciliary arteries with color Doppler was performed. Results. Among women, hemodynamic arterial parameter of the peak-systolic velocity was increased in the central retinal artery and decreased in the ophthalmic artery and posterior ciliary arteries; end- diastolic velocity was increased in all three retrobulbar vascular levels; Pourcelot resistivity index was increased, but pulsatility index was decreased in all three vessels. Among men, peak-systolic velocity, end-diastolic velocity and pulsatility index were decreased in all three vessels; resistivity index was increased in the ophthalmic artery, but decreased in the central retinal artery and posterior ciliary arteries. There was a significant change of the ophthalmic artery pulsatility index in women, and the end-diastolic velocity of the ophthalmic artery in men. Conclusion. There was a difference of the retrobulbar arterial circulation between women and men with primary open angle glaucoma after decrease of the elevated intraocular pressure. The role of vascular factors in the supply of the optic disc neuroretinal rim is important.
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Walcott, Gregory P., Sharon B. Melnick, Cheryl R. Killingsworth, William M. Smith, and Raymond E. Ideker. "Effects of burst stimulation during ventricular fibrillation on cardiac function after defibrillation." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 2 (August 2003): H766—H774. http://dx.doi.org/10.1152/ajpheart.00137.2002.
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The purpose of defibrillation is to rapidly restore blood flow and tissue perfusion following ventricular fibrillation (VF) and shock delivery. We tested the hypotheses that 1) a series of 1-ms pulses of various amplitudes delivered before the defibrillation shock can improve hemodynamics following the shock, and 2) this hemodynamic improvement is due to stimulation of cardiac or thoracic sympathetic nerves. Ten anesthetized pigs received a burst of either 15 or 30 1-ms pulses (0.1–10 A in strength) during VF, after which defibrillation was performed. ECG, arterial blood pressure, and left ventricular (LV) pressure were recorded. Defibrillation shocks and burst pulses were delivered from a right ventricular coil electrode to superior vena cava coil and left chest wall electrodes. Sympathetic blockade was induced with 1 mg/kg timolol and trials were repeated. The first half of this protocol was repeated in two animals that were pretreated with reserpine. Heart rate (HR) after 1-, 2-, 5-, and 10-A pulses was significantly higher than after control shocks without preceding pulse therapy. Mean and peak LV pressure measurements increased 38 and 72%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. Mean and peak arterial pressures increased 36 and 43%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. After β-blockade, HR, mean and peak arterial pressures, and mean LV pressure were not significantly different after pulses of any strength compared with control shocks. LV peak pressure following the 10-A pulses was significantly higher than with no burst pulses but was significantly lower than the response to the 10-A pulses delivered without β-blockade. HR, mean and peak arterial pressures, and mean and peak LV pressure responses after 15 or 30 5- or 10-A pulses were similar to the responses to the same pulses after β-blockade. We conclude that a burst of 15–30 1-ms pulses delivered during VF can increase HR, arterial pressure, and LV pressure following defibrillation. β-Blockade or reserpine pretreatment prevents most of this postshock increase in HR, arterial pressure, and LV pressure.
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Rouby, J. J., M. Houissa, J. F. Brichant, J. F. Baron, C. McMillan, M. Arthaud, P. Amzallag, and P. Viars. "Effects of high-frequency jet ventilation on arterial baroreflex regulation of heart rate." Journal of Applied Physiology 63, no. 6 (December 1, 1987): 2216–22. http://dx.doi.org/10.1152/jappl.1987.63.6.2216.
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Fifteen anesthetized mechanically ventilated patients recovering from multiple trauma were studied to compare the effects of high-frequency jet ventilation (HFJV) and continuous positive-pressure ventilation (CPPV) on arterial baroreflex regulation of heart rate. Systolic arterial pressure and right atrial pressure were measured using indwelling catheters. Electrocardiogram (ECG) and mean airway pressure were continuously monitored. Lung volumes were measured using two linear differential transformers mounted on thoracic and abdominal belts. Baroreflex testing was performed by sequential intravenous bolus injections of phenylephrine (200 micrograms) and nitroglycerin (200 micrograms) to raise or lower systolic arterial pressure by 20–30 Torr. Baroreflex regulation of heart rate was expressed as the slope of the regression line between R-R interval of the ECG and systolic arterial pressure. In each mode of ventilation the ventilatory settings were chosen to control mean airway pressure and arterial PCO2 (PaCO2). In HFJV a tidal volume of 159 +/- 61 ml was administered at a frequency of 320 +/- 104 breaths/min, whereas in CPPV a tidal volume of 702 +/- 201 ml was administered at a frequency of 13 +/- 2 breaths/min. Control values of systolic arterial pressure, R-R interval, mean pulmonary volume above apneic functional residual capacity, end-expiratory pulmonary volume, right atrial pressure, mean airway pressure, PaCO2, pH, PaO2, and temperature before injection of phenylephrine or nitroglycerin were comparable in HFJV and CPPV. Baroreflex regulation of heart rate after nitroglycerin injection was significantly higher in HFJV (4.1 +/- 2.8 ms/Torr) than in CPPV (1.96 +/- 1.23 ms/Torr).(ABSTRACT TRUNCATED AT 250 WORDS)
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Coddens, Jos??, and Thierry Deloof. "End-Systolic Pressure-Volume Relationship and Arterial Elastance." Anesthesia & Analgesia 74, no. 1 (January 1992): 165. http://dx.doi.org/10.1213/00000539-199201000-00032.
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Safar, Michel E., Peter M. Nilsson, Jacques Blacher, and Albert Mimran. "Pulse Pressure, Arterial Stiffness, and End-Organ Damage." Current Hypertension Reports 14, no. 4 (May 4, 2012): 339–44. http://dx.doi.org/10.1007/s11906-012-0272-9.
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Dongare, Dhanashree, Girish S. aundattikar, and Payal Gupta. "Comparison of ventilation with and without positive end expiratory pressure during anesthesia for laparoscopic surgeries." Indian Journal of Clinical Anaesthesia 8, no. 1 (March 15, 2021): 45–48. http://dx.doi.org/10.18231/j.ijca.2021.009.
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Respiratory dynamics are significantly altered during laparoscopic surgeries. Anesthesiologists should be well versed with the benefits as well as limitations of positive end expiratory pressure (PEEP) during laparoscopy. They can then judiciously use the same in different patient populations. In this study we have compared the effects of ventilation with and without PEEP of 10 cm on blood gases, airway pressures and hemodynamic parameters during laparoscopy. 60 patients, from American Society of Anesthesiologists (ASA) physical status I and II, in the age group of 18 to 60, posted for laparoscopic cholecystectomy were enrolled. They were randomized into two groups of 30 each. Group P received PEEP of 10 cm during laparoscopy and group C did not receive any PEEP. The vital parameters, arterial blood gases, and airway pressures were compared in both groups. The oxygenation, (PaO2/FiO2 ratio) was significantly higher in PEEP group (446. 4 ± 113.32 mm of Hg) as compared to the control group (404 ± 51.4 mm of Hg) after one hour of laparoscopy (P= 0.0037). The control group had higher arterial carbon dioxide tension (42.84 ± 2.38 mm of Hg) as compared to PEEP group (41.86 ± 2.33 mm of Hg), (P < 0.001). Both the findings suggest better ventilation perfusion matching in PEEP group. There was a no significant variation in mean arterial pressure and heart rate due to PEEP in our patient population. However the peak airway pressures were significantly higher in PEEP group. 10 cm of PEEP helped in better oxygenation with no significant hemodynamic alterations, in otherwise healthy patients undergoing laparoscopic cholecystectomy.