Wright G, Knecht E, Toraason M
J Appl Physiol Respir Environ Exerc Physiol. 1978 Oct;45(4):521-7. doi: 10.1152/jappl.1978.45.4.521.
The cardiovascular response to severe whole-body heating was examined in anesthetized spontaneously hypertensive (SH) (mean BP = 140 Torr) and normotensive (N) rats (mean BP = 96 Torr). Elevation of colonic temperature to 44 degrees C resulted in an initial increase in arterial pressure (mean BP: SH = 199 Torr, N = 124 Torr) with a subsequent severe hypotension. There was little evidence to suggest that this collapse in systemic pressure was related to a direct heat impairment of cardiac function. It was more likely the result of a progressive venodilation which produced venous pooling and decreased venous return. The arterial blood pressure response to exogenous catecholamine challenge decreased at elevated temperatures. This suggests that there was a deterioration of the vasoconstrictor response and indicated a possible effect of heat at the receptor or effector level. There were significant differences between the responses of normotensive and hypertensive rats to whole-body heating suggesting an enhanced cardiovascular sensitivity in hypertensive rats that may partially explain earlier reports of inferior thermoregulation and heat intolerance in these animals.
在麻醉状态下的自发性高血压（SH）大鼠（平均血压 = 140 托）和正常血压（N）大鼠（平均血压 = 96 托）中，研究了对严重全身加热的心血管反应。将结肠温度升高至 44 摄氏度会导致动脉压最初升高（平均血压：SH = 199 托，N = 124 托），随后出现严重低血压。几乎没有证据表明全身血压的这种崩溃与心脏功能的直接热损伤有关。它更可能是渐进性静脉扩张的结果，这种扩张导致静脉淤血并减少静脉回流。在温度升高时，对外源性儿茶酚胺刺激的动脉血压反应降低。这表明血管收缩反应恶化，并表明热在受体或效应器水平可能产生影响。正常血压和高血压大鼠对全身加热的反应存在显著差异，这表明高血压大鼠的心血管敏感性增强，这可能部分解释了这些动物早期关于体温调节较差和不耐热的报道。
