BLOOD VOLUME AND VENOUS RETURN IN THERMAL STRAIN

该项目的长期目标是揭示 提供维持心脏功能的生理机制 足够的静脉回流，因此有足够的心脏充盈 压力，在人体热紧张的条件下。我们的特定 未来五年的目标如下： 1)设计并验证将定义角色的技术 静脉流出阻力变化在血液测定中的应用 在运动和/或热应激期间依赖的静脉中聚集。 2)确定提供血容量的机制 已知的是伴随着体育锻炼而来的扩张。我们假设 这些涉及心肺压力感受器反射的减少 灵敏度和合成血浆的能力的增加 蛋白质。 3)确定急性血容量扩张是否会改变 外周血管收缩反应对体外循环的影响 压力感受器卸载，从而模拟物理的影响 训练。 4)描述体液隔间的移位 在运动期间，用不同的溶液进行复水 钠浓度。我们假设饮用稀释的盐水 锻炼期间会对身体提供更好的维护，S 水平衡和血容量也是如此。 为了实现这些目标，我们将研究环流 人体志愿者在运动、重力作用下的反应 下半身负压引起的应激，以及在 进行性脱水。我们将把循环反应联系起来 (例如，前臂血管对主动脉阻力的变化 生理刺激(例如中心静脉压的变化) 这些研究。我们将在条件下研究这些志愿者 他们的血液容量被人为地操纵，通过 血清白蛋白输注，自然是有氧运动的结果 训练。我们希望了解这些物理因素 有助于外周和血液的汇集 反对静脉淤积的生理因素。这些 研究应该提高我们对动脉控制的理解 应该提供关于血压的新知识 人类在以下情况下抵抗晕厥的机制 静脉回流减少。

The long-term objectives of this project are to uncover the physiological mechanisms that provide for the maintenance of an adequate venous return, and therefore an adequate cardiac filling pressure, in conditions of thermal strain in humans. Our specific aims over the next five years are as follows: 1) to devise and validate a technique that will define the role of venous outflow resistance changes in the determination of blood pooling in dependent veins during exercise and/or heat stress. 2) to determine the mechanisms that provide for the blood volume expansion known to accompany physical training. We hypothesize that these involve a decrease in cardiopulmonary baroreflex sensitivity and an increase in the capacity to synthesize plasma proteins. 3) to determine whether acute blood volume expansion will modify the peripheral vasoconstrictor response to cardiopulmonary baroreceptor unloading and thereby mimic the effects of physical training. 4) to characterize the shifts in the body fluid compartments during exercise while rehydrating with solutions of different sodium concentrations. We hypothesize that drinking dilute saline during exercise will provide a better maintenance of the body,s water balance and of blood volume as well. In order to accomplish these aims, we will study the circulatory responses of human volunteers during exercise, during gravitational stress induced by lower body negative pressure, and during progressive dehydration. We will relate the circulatory responses (e.g. change in forearm vascular resistance to the primary physiological stimuli (e.g. change in central venous pressure) in these studies. We will study these volunteers in conditions in which their blood volumes have been manipulated artificially, by serum albumin infusion, and naturally, as a result of aerobic training. We expect to learn about the physical factors that contribute to the pooling of blood in the periphery and the physiological factors that act to oppose venous pooling. These studies should improve our understanding of the control of arterial blood pressure and should provide new knowledge about the mechanisms that humans employ to resist syncope in conditions of reduced venous return.