The magnitude of heat stress-induced reductions in cerebral perfusion does not predict heat stress-induced reductions in tolerance to a simulated hemorrhage

摘要

Although all humans experience reduced tolerance to hypovo-lemia and exhibit impaired blood pressure control when heat stressed, the degree of reduction in these responses varies greatly among individuals (3). Furthermore, the mechanisms responsible for this variability are multifaceted and poorly understood. Despite the precise mechanisms, syncope will always occur when cerebral perfusion becomes inadequate. Indeed, cerebral perfusion is reduced during heat stress compared with normothermic conditions (4, 6, 30, 47) and, therefore, may reduce tolerance to a simulated hemorrhage by lowering the functional reserve by which cerebral perfusion can be further reduced before ensuing syncopal symptoms develop, hi this regard, it is plausible that individuals with the greatest heat stress-induced reductions in tolerance to a simulated hemorrhage may have the largest reduction in cerebral perfusion during heat stress. Additionally, tolerance during an orthostatic challenge in normothermic conditions is positively related to the magnitude of activation of the RAAS and subsequent increases in circulating angiotensin II (ANG II) (16, 17, 19). Heat stress also results in activation of the RAAS (15). Thus individuals with a larger increase in plasma ANG II in response to heat stress would be expected to have increased tolerance to a simulated hemorrhage challenge during heat stress conditions.