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Systemic Arterial Pressure (systemic + arterial_pressure)
Selected AbstractsThe baroreflex is counteracted by autoregulation, thereby preventing circulatory instabilityEXPERIMENTAL PHYSIOLOGY, Issue 4 2004Roberto Burattini The aims of this study were (a) to apply in the animal with intact baroreflex a two-point method for estimation of overall, effective open-loop gain, G0e, which results from the combined action of baroregulation and total systemic autoregulation on peripheral resistance; (b) to predict specific baroreflex gain by correcting the effective gain for the autoregulation gain; and (c) to discuss why the effective gain is usually as low as 1,2 units. G0e was estimated from two measurements of both cardiac output, Q, and mean systemic arterial pressure, P: one in the reference state (set-point) and the other in a steady-state reached 1,3 min after a small cardiac output perturbation. In anaesthetized cats and dogs a cardiac output perturbation was accomplished by partial occlusion of the inferior vena cava and by cardiac pacing, respectively. Average (±s.e.m.) estimates of G0e were 1.4 ± 0.2 (n= 8) in the cat and 1.5 ± 0.4 (n= 5) in the dog. The specific baroreflex open-loop gain, G0b, found after correction for total systemic autoregulation, was 3.3 ± 0.4 in the cat and 2.8 ± 0.8 in the dog. A model-based analysis showed that, with G0e as low as 1.4, the closed-loop response of P to a stepwise perturbation in Q results in damped oscillations that disappear in about 1 min. The amplitude and duration of these oscillations, which have a frequency of about 0.1 Hz, increase with increasing G0e and cause instability when G0e is about 3. We conclude that autoregulation reduces the effectiveness of baroreflex gain by about 55%, thereby preventing instability of blood pressure response. [source] Clinical methods for the evaluation of endothelial function , a focus on resistance arteriesFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 3 2006Robinson Joannides Abstract Endothelial dysfunction is a key event in the pathophysiology of cardiovascular diseases and appears as a strong independent predictor of cardiovascular events. In this context, biological evaluation of endothelial circulating markers can be helpful. However, functional tests using pharmacological stimuli appear more specific for the study of resistance arteries. These methods consist in the evaluation of the endothelium-dependent changes in regional vascular flow in response to local infusion of substances that act through endothelial receptors without modification of systemic arterial pressure and in comparison with a non endothelium-dependent relaxation. Flow is measured by Doppler and intravascular ultrasound in coronary circulation, laser Doppler in skin and by venous occlusion plethysmography in peripheral muscular arteries. Similar studies can be performed ex vivo using isolated resistance arteries obtained from fat subcutaneous biopsies. In addition, other information can be obtained from reactive hyperemia and the study of the flow-mediated dilatation of conduit arteries to enable a selective and comprehensive approach of the heterogeneity of endothelial function in pathophysiology. [source] The Role of the Kidneys in HypertensionJOURNAL OF CLINICAL HYPERTENSION, Issue 9 2005L. Gabriel Navar PhD The devastating long-term consequences of high blood pressure include stroke, heart disease, atherosclerosis, renal disease, and other end-organ damage. From a physiologic perspective, it is not apparent why the propensity for hypertension is so widespread in the general population. Clearly, an adequate arterial pressure is essential for perfusion of the tissues to provide adequate oxygenation and nutrition to the brain and other critical organs. Although the various microcirculatory beds have the capability to adjust vascular resistance to autoregulate blood flow, systemic arterial pressure is usually maintained at levels greater than required for requisite tissue perfusion. The myriad of neurohumoral mechanisms designed to protect against decreases in systemic arterial pressure provide a reserve capacity for increased perfusion when there are increased tissue demands. The unfortunate consequence of having these powerful physiologic control mechanisms is that they may be inappropriately activated in certain circumstances or by genetically determined traits, leading to hypertension and cardiovascular injury. Evidence continues to accumulate indicating that the kidney not only is victim to hypertension-related injury, but also contributes as a villain to the hypertensinogenic process. [source] Hemodynamic profile and tissular oxygenation in orthotopic liver transplantation: Influence of hepatic artery or portal vein revascularization of the graftLIVER TRANSPLANTATION, Issue 11 2006Carlos Moreno We performed a prospective, randomized study of adult patients undergoing orthotopic liver transplantation, comparing hemodynamic and tissular oxygenation during reperfusion of the graft. In 30 patients, revascularization was started through the hepatic artery (i.e., initial arterial revascularization) and 10 minutes later the portal vein was unclamped; in 30 others, revascularization was started through the portal vein (i.e., initial portal revascularization) and 10 minutes later the hepatic artery was unclamped. The primary endpoints of the study were mean systemic arterial pressure and the gastric-end-tidal carbon dioxide partial pressure (PCO2) difference. The secondary endpoints were other hemodynamic and metabolic data. The pattern of the hemodynamic parameters and tissue oxygenation values during the dissection and anhepatic stages were similar in both groups At the first unclamping, initial portal revascularization produced higher values of mean pulmonary pressure (25 ± 7 mm of Hg vs. 17 ± 4 mm of Hg; P < 0.05) and wedge and central venous pressures. At the second unclamping, initial portal revascularization produced higher values of cardiac output and mean arterial pressure (87 ± 15 mm of Hg vs. 79 ± 15 mm of Hg; P < 0.05) and pulmonary blood pressure. Postreperfusion syndrome was present in 13 patients (42.5%) in the arterial group and in 11 patients (36%) in the portal group. During revascularization, the values of gastric and arterial pH decreased in both groups and recovered at the end of the procedure, but were more accentuated in the initial arterial revascularization group. In conclusion, we found that initial arterial revascularization of the graft increases pulmonary pressure less markedly, so it may be indicated for those patients with poor pulmonary and cardiac reserve. Nevertheless, for the remaining patients, initial portal revascularization offers more favorable hemodynamic and metabolic behavior, less inotropic drug use, and earlier normalization of lactate and pH values. Liver Transpl, 2006. © 2006 AASLD. [source] Reverse flow facial artery as recipient vessel for perforator flapsMICROSURGERY, Issue 6 2009D.D.S., Frank Hölzle M.D., Ph.D. In perforator flaps, anastomosis between flap and recipient vessels in the neck area is often difficult due to small vessel diameter and short pedicle. The aim of this study was to investigate whether the retrograde flow of the distal, paramandibular part of the facial artery would provide sufficient pressure and size to perfuse perforator flaps. Before and after occlusion of the contralateral facial artery, retrograde and anterograde arterial pressure was measured on both sides of the facial artery in 50 patients. The values were compared with the mean systemic arterial pressure. Diameters of facial arteries in the paramandibular region and perforator flap vessels were evaluated by morphometry. Arterial pressure in the distal facial artery with retrograde flow was 76% of the systemic arterial pressure. The latter equaled approximately the anterograde arterial pressure in the proximal end of the facial artery. Mean arterial pressure of the facial arteries decreased after proximal occlusion of the contralateral facial artery, which was not significant (P = 0.09). Mean diameter of the distal facial arteries in the mandibular region was 1.6 mm (range 1.3,2.2 mm; standard deviation 0.3 mm; n = 50), that of the perforator flap arteries 1.3 mm (0.9,2.6 mm; 0.4 mm; n = 20). Facial arteries, based on reverse flow, successfully supported all 20 perforator flaps. Retrograde pulsatile flow in the distal facial artery sustains perforator flaps even if the contralateral facial artery is occluded. Proximity of the distal facial arteries to the defect compensates for short pedicles. Matching diameters of the arteries are ideal for end-to-end anastomosis. © 2009 Wiley-Liss, Inc. Microsurgery, 2009. [source] Splanchnic vasoconstriction by angiotensin II is arterial pressure dependentACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 1 2002M. Broomé Background: Our hypothesis was that splanchnic vasoconstriction by exogenous angiotensin II (Ang II) is significantly potentiated by local mechanisms increasing vasomotor tone and that splanchnic tissue oxygenation during administration of Ang II is perfusion pressure dependent. The aim was to study local splanchnic circulatory effects and tissue oxygenation during intravenous infusion of Ang II at different levels of regional arterial driving pressure in a whole-body large animal model. Methods: Ang II was infused in incremental doses (0,200 ,g,·,h,1) in anaesthetised instrumented pigs (n=8). Mean superior mesenteric arterial pressure (PSMA) was adjusted by a local variable perivascular occluder. Perivascular ultrasound and laser-Doppler flowmetry were used for measurements of mesenteric venous blood flow and superficial intestinal blood flow, respectively. Intestinal oxygenation was evaluated by oxygen tissue tension (PtiO2) and lactate fluxes. Results: Ang II produced prominent and dose-dependent increases in mesenteric vascular resistance (RSMA) when the intestine was exposed to systemic arterial pressure, but Ang II increased RSMA only minimally when PSMA was artificially kept constant at a lower level (50 mmHg) by the occluder. Although Ang II decreased PtiO2 at a PSMA of 50 mmHg, splanchnic lactate production was not observed. Conclusion: We demonstrate that splanchnic vasoconstriction by exogenous Ang II is dependent on arterial driving pressure, suggesting significant potentiation through autoregulatory increases in vasomotor tone. Intestinal hypoxaemia does not seem to occur during short-term infusion of Ang II in doses that significantly increases systemic arterial pressure. [source] Contribution of pulmonary surfactant with inhaled nitric oxide for treatment of pulmonary hypertensionPEDIATRICS INTERNATIONAL, Issue 5 2006SATOSHI KUSUDA Abstract Background: Combined therapy of inhaled nitric oxide (iNO) with pulmonary surfactant replacement was reported to improve oxygenation in patients or animal models of persistent pulmonary hypertension of the newborn with pulmonary surfactant deficiency lung. To evaluate the potential of iNO for the treatment of persistent pulmonary hypertension of the newborn, pulmonary arterial pressure (PAP) was measured during iNO before and after pulmonary surfactant replacement in an animal model of pulmonary hypertension with surfactant deficiency. Methods: Seven newborn piglets were injected with L-nitro-arginine-methylester to produce an animal model of pulmonary hypertension. After PAP increased, iNO (30 p.p.m.) was introduced. Then iNO was stopped, and animals were subjected to lung lavage with saline. After recording the effect of iNO, all animals then received exogenous pulmonary surfactant installation. After surfactant treatment, iNO was again introduced. Results: Pulmonary arterial pressure and systemic arterial pressure were increased significantly by >30% after infusion of L-nitro-arginine-methylester. During iNO only PAP was reduced significantly. Respiratory system compliance decreased significantly after lung lavage, and increased significantly after pulmonary surfactant replacement with concomitant increase of PaO2. In contrast, significant reduction of PAP with iNO before and after pulmonary surfactant replacement were also observed. The reduction ratios of PAP under each condition were 75.2 ± 7.4%, 81.3 ± 3.1%, and 79.1 ± 5.3%, respectively (not significant among conditions). Conclusion: These results suggest that iNO is still a potent pulmonary arterial vasodilator even under pulmonary surfactant deficiency in an animal model of pulmonary hypertension. [source] Fully Autonomous Preload-Sensitive Control of Implantable Rotary Blood PumpsARTIFICIAL ORGANS, Issue 9 2010Andreas Arndt Abstract A pulsatility-based control algorithm with a self-adapting pulsatility reference value is proposed for an implantable rotary blood pump and is to be tested in computer simulations. The only input signal is the pressure difference across the pump, which is deduced from measurements of the pump's magnetic bearing. A pulsatility index (PI) is calculated as the mean absolute deviation from the mean pressure difference. As a second characteristic, the gradient of the PI with respect to the pump speed is derived. This pulsatility gradient (GPI) is used as the controlled variable to adjust the operating point of the pump when physiological variables such as the systemic arterial pressure, left ventricular contractility, or heart rate change. Depending on the selected mode of operation, the controller is either a linear controller or an extremum-seeking controller. A supervisory mechanism monitors the state of the system and projects the system into the region of convergence when necessary. The controller of the GPI continuously adjusts the reference value for PI. An underlying robust linear controller regulates the PI to the reference value in order to take into account changes in pulmonary venous return. As a means of reacting to sudden changes in the venous return, a suction detection mechanism was included. The control system is robustly stable within a wide range of physiological variables. All the clinician needs to do is to select between the two operating modes. No other adjustments are required. The algorithm showed promising results which encourage further testing in vitro and in vivo. [source] | ||||||||||