Heat defense control in an experimental heat disorder.
Heat defense control in an experimental heat disorder.
复制标题
实验性热紊乱中的热防御控制。
DOI：
10.1007/s004840050005
复制
发表时间：
2000
影响因子：
3.2
通讯作者：
Blatteis,CM
中科院分区：
文献类型：
--
作者：
Romanovsky,AA;Blatteis,CM
Both whole-body heat exposure and intraperitoneal heating (IPH) result in a body temperature (Tb) fall that occurs once heating is abated (”hyperthermia- induced hypothermia”). This phenomenon involves a decrease in the thresholdTb(Tb-thresh) for activation of metabolic heat production (cold defense). Whether theTb-threshfor ear skin vasodilation (heat defense) also changes during hyperthermia-induced hypothermia remains unknown. In experiment 1, we applied IPH to guinea pigs by perfusing water through a preimplanted intraperitoneal thermode and delivered the total heat load of either approximately 1.5 kJ (”short” IPH; perfusion duration: 14 min) or approximately 3.0 kJ (”long” IPH; 40 min). Short IPH caused skin vasodilation and a 1.1°C rise inTb; no hypothermia occurred when IPH ceased. Long IPH caused vasodilation and hyperthermia of a comparable magnitude (1.4°C) that were followed by aTbfall to 1.9°C below the preheating value. In experiment 2, theTb-threshfor skin vasodilation was measured twice: at the beginning of long IPH and at the nadir of the post-IPH hypothermia. The twoTb-threshvalues were 39.0 (SEM 0.1)°C and 39.2 (SEM 0.2)°C respectively. In the controls, theTb-threshwas measured at the beginning and after short IPH; both control values were 39.0 (SEM 0.2)°C. We conclude that the hyperthermia- induced hypothermia, although previously shown to be coupled with a decrease in theTb-threshfor cold defense, occurs without any substantial change in theTb-threshfor heat defense. We speculate that postheating thermoregulatory disorders are associated with threshold dissociation, thus representing the poikilothermic (wide dead-band) type ofTbcontrol.
