Wilkinson M F, Kasting N W
Department of Physiology, Faculty of Medicine, University of British Columbia, Vancouver, Canada.
Regul Pept. 1987 Oct;19(1-2):45-54. doi: 10.1016/0167-0115(87)90073-5.
The intracerebroventricular (i.c.v.) administration of arginine vasopressin (AVP), in the febrile rat elicits an antipyresis at cold, warm and neutral ambient temperatures. These experiments were conducted, therefore, to elucidate the thermoregulatory effector mechanisms responsible for this antipyretic effect. At 25 degrees C, AVP-induced antipyresis was mediated by tail skin vasodilation while metabolic rate was unaffected. At 4 degrees C, the antipyresis produced by AVP was approximately double that seen at 25 degrees C. This effect appeared to be mediated exclusively by inhibition of heat production since the metabolic rate decreased markedly following AVP. This antipyresis at 4 degrees C was accompanied by cutaneous vasoconstriction. At 32 degrees C, neither vasomotor tone, metabolic rate nor evaporative heat loss could be shown to contribute to the small antipyretic effect elicited by AVP. We conclude from these data that i.c.v. AVP is producing antipyresis by affecting the febrile body temperature set-point mechanism since the thermoregulatory strategy to lose heat varies at different ambient temperatures and the decrease in body temperature cannot be shown to be due to changes in a single effector mechanism.
在发热大鼠中，脑室内（i.c.v.）注射精氨酸加压素（AVP），在寒冷、温暖和中性环境温度下均可引起解热作用。因此，进行了这些实验以阐明导致这种解热作用的体温调节效应机制。在25摄氏度时，AVP诱导的解热作用是通过尾部皮肤血管舒张介导的，而代谢率未受影响。在4摄氏度时，AVP产生的解热作用约为25摄氏度时的两倍。这种作用似乎完全是通过抑制产热介导的，因为AVP注射后代谢率显著降低。在4摄氏度时的这种解热作用伴有皮肤血管收缩。在32摄氏度时，血管运动张力、代谢率或蒸发散热均未显示对AVP引起的微小解热作用有贡献。我们从这些数据得出结论，脑室内注射AVP通过影响发热体温设定点机制产生解热作用，因为在不同环境温度下散热的体温调节策略不同，且体温降低并非单一效应机制变化所致。
