Lomax P, Lee R J
Eur J Pharmacol. 1982 Oct 15;84(1-2):87-91. doi: 10.1016/0014-2999(82)90160-1.
The fall in core temperature induced by a fixed dose of ethanol (1 g x kg-1 i.p.) was an exponential function of the ambient temperature over the range 0-18 degrees C. In rats acclimated to 4 degrees C for 7 days the dose response curve relating the fall in body temperature to ethanol was markedly attenuated. The hypothermic effect of ethanol declined exponentially over 20 days of exposure to 4 degrees C and by the 20th day the fall was no greater than in saline injected controls. Blood ethanol concentrations were similar in acclimated and non-acclimated rats indicating that pharmacokinetic factors do not account for the altered responses. Although the time course of the development of resistance to the hypothermic effect of ethanol parallels that of cold acclimation to 4 degrees C, and the development of non-shivering thermogenesis, the attenuated drug effect does not appear to be due to the altered metabolic activity of brown adipose tissue. It is suggested that the modulation of the effect of ethanol in lowering the thermoregulatory set point results from central nervous system adaptation to the environmental thermal stress.
固定剂量乙醇（1克/千克腹腔注射）引起的核心体温下降在0至18摄氏度范围内是环境温度的指数函数。在适应4摄氏度环境7天的大鼠中，与乙醇相关的体温下降剂量反应曲线明显减弱。在暴露于4摄氏度环境20天的过程中，乙醇的体温过低效应呈指数下降，到第20天时，体温下降幅度不大于注射生理盐水的对照组。适应和未适应的大鼠血液乙醇浓度相似，表明药代动力学因素不能解释反应的改变。尽管对乙醇体温过低效应产生抗性的时间进程与对4摄氏度冷适应以及非寒战产热的时间进程相似，但药物效应减弱似乎并非由于棕色脂肪组织代谢活性的改变。提示乙醇降低体温调节设定点的效应受到调节是由于中枢神经系统适应环境热应激所致。
