Wasserstrum N, Herd J A
Am J Physiol. 1977 May;232(5):H451-8. doi: 10.1152/ajpheart.1977.232.5.H451.
Unanesthetized squirrel monkeys exposed to an ambient temperature of 10 degrees C showed elevations in total body oxygen consumption (VO2), arterial blood pressure (BP), and heart rate (HR) above values recorded at 28 degrees C. Further elevation of BP in the cold by intravenous infusion of phenylephrine was accompanied by immediate reduction in VO2, inhibition of shivering, and decrease in rectal temperature, as well as immediate reduction in HR. The magnitude of reduction in VO2 correlated with the magnitude of the concomitant baroreflexive bradycardia. When the pressor effects of phenylephrine were opposed by administration of diazoxide or phentolamine, the inhibitory effects of phenylephrine on both HR and VO2 were abolished. In animals previously subjected to bilateral sinoaortic denervation, both the bradycardia and depression in oxygen consumption normally associated with BP elevation were markedly reduced. These results suggest that elevation of blood pressuere can inhibit the thermoregulatory increase in total body oxygen consumption normally produced by cold exposure, and that this inhibition, like the concomitant bradycardia, is probably mediated via the sinoaortic baroreceptors.
暴露于10摄氏度环境温度下的未麻醉松鼠猴,其全身氧耗量(VO2)、动脉血压(BP)和心率(HR)均高于在28摄氏度时记录的值。通过静脉输注去氧肾上腺素使寒冷环境中的血压进一步升高,同时伴有VO2立即降低、寒战抑制、直肠温度下降以及HR立即降低。VO2降低的幅度与伴随的压力反射性心动过缓的幅度相关。当用二氮嗪或酚妥拉明对抗去氧肾上腺素的升压作用时,去氧肾上腺素对HR和VO2的抑制作用均被消除。在先前接受双侧窦主动脉去神经支配的动物中,通常与血压升高相关的心动过缓和氧耗量降低均明显减轻。这些结果表明,血压升高可抑制寒冷暴露通常引起的全身氧耗量的体温调节性增加,并且这种抑制作用,与伴随的心动过缓一样,可能是通过窦主动脉压力感受器介导的。