Oufara S, Veillat J P, El Hilali M
J Physiol (Paris). 1980;76(2):167-71.
The survival of rats acclimatized to either 5 degrees C or 30 degrees C, treated or not with propylthiouracil (P.T.U.), was determined at 40 degrees C. Changes in metabolic rate and rectal temperature were followed throughout exposure. Total water loss was estimated at the end of the experiment. The survival time of rats accclimatized to 5 degrees C was less than that of rats acclimatized to 30 degrees C, and that of controls was less than that of treated animals. The differences reported seem to be independent of heat transfer capacities, which are similar in all treatment conditions and possibly limited by the experimental set up. A high thermogenic rate would appear to limit resistance to heat under conditions where external heat stress approaches heat transferability, such that the animal's temperature overcomes the lethal threshold, and leads to heat stroke. Results of P.T.U. treatment suggest the involvement of thyroid hormones in heat stress-induced thermogenesis and in cellular lability to elevated internal temperatures.
测定了适应5摄氏度或30摄氏度环境、接受或未接受丙硫氧嘧啶（P.T.U.）处理的大鼠在40摄氏度环境下的存活率。在整个暴露过程中跟踪代谢率和直肠温度的变化。实验结束时估算总失水量。适应5摄氏度环境的大鼠的存活时间短于适应30摄氏度环境的大鼠，对照组大鼠的存活时间短于接受处理的动物。所报告的差异似乎与热传递能力无关，热传递能力在所有处理条件下相似，并且可能受实验设置限制。在外部热应激接近热传递能力的条件下，高热生成率似乎会限制对热的抵抗力，从而使动物体温超过致死阈值并导致中暑。丙硫氧嘧啶处理的结果表明甲状腺激素参与了热应激诱导的产热以及细胞对内部温度升高的易损性。
