Home About us Contact
|
Home About us Contact | ||
|
|
||
Short-term Regulation (short-term + regulation)
Selected AbstractsEffect of angiotensin II and endothelin-1 receptor blockade on the haemodynamic and hormonal changes after acute blood loss and after retransfusion in conscious dogsACTA PHYSIOLOGICA, Issue 4 2004R. C. E. Francis Abstract Aim:, This study investigates angiotensin II and endothelin-1 mediated mechanisms involved in the haemodynamic, hormonal, and renal response towards acute hypotensive haemorrhage. Methods:, Conscious dogs were pre-treated with angiotensin II type 1 (AT1) and/or endothelin-A (ETA) receptor blockers or not. Protocol 1: After a 60-min baseline period, 25% of the dog's blood was rapidly withdrawn. The blood was retransfused 60 min later and data recorded for another hour. Protocol 2: Likewise, but preceded by AT1 blockade with i.v. Losartan. Protocol 3: Likewise, but preceded by ETA blockade with i.v. ABT-627. Protocol 4: Likewise, but with combined AT1plus ETAblockade. Results:, In controls, haemorrhage decreased mean arterial pressure (MAP) by approximately 25%, cardiac output by approximately 40%, and urine volume by approximately 60%, increased angiotensin II (3.1-fold), endothelin-1 (1.13-fold), vasopressin (116-fold), and adrenaline concentrations (3.2-fold). Glomerular filtration rate and noradrenaline concentrations remained unchanged. During AT1 blockade, the MAP decrease was exaggerated (,40%) and glomerular filtration rate fell. During ETA blockade, noradrenaline increased after haemorrhage instead of adrenaline, and the MAP recovery after retransfusion was blunted. The decrease in cardiac output was similar in all protocols. Conclusions:, Angiotensin II is more important than endothelin-1 for the short-term regulation of MAP and glomerular filtration rate after haemorrhage, whereas endothelin-1 seems necessary for complete MAP recovery after retransfusion. After haemorrhage, endothelin-1 seems to facilitate adrenaline release and to blunt noradrenaline release. Haemorrhage-induced compensatory mechanisms maintain blood flow more effectively than blood pressure, as the decrease in cardiac output , but not MAP , was similar in all protocols. [source] Transpiration and stomatal conductance across a steep climate gradient in the southern Rocky MountainsECOHYDROLOGY, Issue 3 2008Nate G. McDowell Abstract Transpiration (E) is regulated over short time periods by stomatal conductance (Gs) and over multi-year periods by tree- and stand-structural factors such as leaf area, height and density, with upper limits ultimately set by climate. We tested the hypothesis that tree structure, stand structure and Gs together regulate E per ground area (Eg) within climatic limits using three sites located across a steep climatic gradient: a low-elevation Juniperus woodland, a mid-elevation Pinus forest and a high-elevation Picea forest. We measured leaf area : sapwood area ratio (Al : As), height and ecosystem sapwood area : ground area ratio (As : Ag) to assess long-term structural adjustments, tree-ring carbon isotope ratios (,13C) to assess seasonal gas exchange, and whole-tree E and Gs to assess short-term regulation. We used a hydraulic model based on Darcy's law to interpret the interactive regulation of Gs and Eg. Common allometric dependencies were found only in the relationship of sapwood area to diameter for pine and spruce; there were strong site differences for allometric relationships of sapwood area to basal area, Al : As and As : Ag. On a sapwood area basis, E decreased with increasing elevation, but this pattern was reversed when E was scaled to the crown using Al : As. Eg was controlled largely by As : Ag, and both Eg and Gs declined from high- to low-elevation sites. Observation-model comparisons of Eg, Gs and ,13C were strongest using the hydraulic model parameterized with precipitation, vapour pressure deficit, Al : As, height, and As : Ag, supporting the concept that climate, Gs, tree- and stand-structure interact to regulate Eg. Copyright © 2008 John Wiley & Sons, Ltd. [source] A sympathetic view of the sympathetic nervous system and human blood pressure regulationEXPERIMENTAL PHYSIOLOGY, Issue 6 2008Michael J. Joyner New ideas about the relative importance of the autonomic nervous system (and especially its sympathetic arm) in long-term blood pressure regulation are emerging. It is well known that mean arterial blood pressure is normally regulated in a fairly narrow range at rest and that blood pressure is also able to rise and fall ,appropriately' to meet the demands of various forms of mental, emotional and physical stress. By contrast, blood pressure varies widely when the autonomic nervous system is absent or when key mechanisms that govern it are destroyed. However, 24 h mean arterial pressure is still surprisingly normal under these conditions. Thus, the dominant idea has been that the kidney is the main long-term regulator of blood pressure and the autonomic nervous system is important in short-term regulation. However, this ,renocentric' scheme can be challenged by observations in humans showing that there is a high degree of individual variability in elements of the autonomic nervous system. Along these lines, the level of sympathetic outflow, the adrenergic responsiveness of blood vessels and individual haemodynamic patterns appear to exist in a complex, but appropriate, balance in normotension. Furthermore, evidence from animals and humans has now clearly shown that the sympathetic nervous system can play an important role in longer term blood pressure regulation in both normotension and hypertension. Finally, humans with high baseline sympathetic traffic might be at increased risk for hypertension if the ,balance' among factors deteriorates or is lost. In this context, the goal of this review is to encourage a comprehensive rethinking of the complexities related to long-term blood pressure regulation in humans and promote finer appreciation of physiological relationships among the autonomic nervous system, vascular function, ageing, metabolism and blood pressure. [source] Cool dialysate reduces asymptomatic intradialytic hypotension and increases baroreflex variabilityHEMODIALYSIS INTERNATIONAL, Issue 2 2009Lindsay J. CHESTERTON Abstract Intradialytic hypotension (IDH) remains an important cause of morbidity and mortality in chronic hemodialysis (HD) patients and can be ameliorated by cool temperature HD. The baroreflex arc is under autonomic control and is essential in the short-term regulation of blood pressure (BP). This study aimed to investigate if the baroreflex sensitivity (BRS) response to HD differed between standard and cool-temperature dialysate. Ten patients (mean age 67±2 years) prone to IDH were recruited into a randomized, crossover study to compare BRS variation at dialysate temperatures of 37 °C (HD37) and 35 °C (HD35). Each patient underwent continuous beat-to-beat BP monitoring during a dialysis session of HD37 and HD35. During HD37 2 patients developed symptomatic IDH, as opposed to 1 with HD35. However, asymptomatic IDH occurred with a frequency of 0.4 episodes per session with HD35 and 6.2 episodes per session during HD37 (odds ratio15.5; 95%CI 5.6,14.2). Although absolute BRS measurements did not differ between the 2 modalities, BRS variability increased during HD35. Our study has demonstrated that in IDH-prone patients, cool HD resulted in a reduction in heart rate and a greater reduction in cardiac output and stroke volume. Mean arterial pressure was maintained through a significantly greater increase in total peripheral resistance. Furthermore, although absolute BRS values during HD were not significantly altered by a reduction in dialysate temperature, there was a greater percentage increase in BRS values during cool HD. Understanding the varied causes of, and categorizing impaired hemodynamic responses to HD will enable further individualization of HD prescriptions according to patient need. [source] | ||||||||||