Spiers D E, Threatte R M, Fregly M J
Pharmacology. 1984;28(3):155-70. doi: 10.1159/000137957.
Several thermoregulatory responses (i.e., colonic temperature, tail-skin temperature, rate of oxygen consumption) were measured in the rat following acute administration of either saline or 3 g ethanol/kg BW i.p. at ambient temperatures (Ta) of 17, 25, and 32 degrees C. The magnitude of the ethanol-induced, hypothermic response was inversely related to Ta, with the decrease in colonic temperature (Tco) at 120 min postinjection ranging from 0.1 degree C at Ta 32 degrees C to 3.2 degrees C at Ta 17 degrees C. Depression of rate of oxygen consumption (heat production) was a major factor contributing to ethanol-induced hypothermia, with no observed differences in heat loss as assessed by differences in the responses of tail skin temperature. Thermoregulatory responses were also measured following acute administration of ethanol at Ta 25 degrees C and immediate exposure to either Ta 32 or 17 degrees C. The increase in Tco of ethanol-treated rats was delayed compared to controls following exposure to 32 degrees C. In addition, tail skin temperature and rate of oxygen consumption of treated rats were significantly lower. The delayed rise in Tco is most likely the result of a reduction in rate of oxygen consumption. When administered ethanol at Ta 25 degrees C and then exposed to Ta 17 degrees C, the rats exhibited a significant recovery from the metabolic depression that characterized the administration of ethanol during exposure to Ta 17 degrees C. This was most likely related to differences in the clearance of ethanol from blood. The results of this study are consistent with the suggestion that the physiologically significant inhibitory effect of acute administration of 3 g ethanol/kg BW on thermoregulatory responses of rats is manifested at the level of heat production rather than heat loss and that the effect is exacerbated by a reduction in Ta.
在17、25和32摄氏度的环境温度（Ta）下，给大鼠腹腔注射生理盐水或3 g乙醇/千克体重后，测量了几种体温调节反应（即结肠温度、尾皮温度、耗氧率）。乙醇诱导的体温过低反应的幅度与Ta呈负相关，注射后120分钟时结肠温度（Tco）的下降幅度在Ta为32摄氏度时为0.1摄氏度，在Ta为17摄氏度时为3.2摄氏度。耗氧率（产热）的降低是乙醇诱导体温过低的主要因素，通过尾皮温度反应的差异评估，未观察到热损失的差异。在Ta为25摄氏度时急性给予乙醇并立即暴露于Ta为32或17摄氏度后，也测量了体温调节反应。与对照组相比，暴露于32摄氏度后，乙醇处理大鼠的Tco升高延迟。此外，处理大鼠的尾皮温度和耗氧率显著降低。Tco的延迟升高很可能是耗氧率降低的结果。当在Ta为25摄氏度时给予乙醇，然后暴露于Ta为17摄氏度时，大鼠从代谢抑制中显著恢复，这种代谢抑制是在暴露于Ta为17摄氏度期间给予乙醇的特征。这很可能与乙醇从血液中的清除差异有关。本研究结果与以下观点一致：急性给予3 g乙醇/千克体重对大鼠体温调节反应的生理显著抑制作用在产热水平而非热损失水平表现出来，并且这种作用会因Ta降低而加剧。
