血管收缩与右旋苯丙胺诱导的体温过低
Vasoconstriction and d-amphetamine-induced hypothermia.
作者信息
Yehuda S, Carasso R L, Ben-Uriah Y
出版信息
Int J Neurosci. 1981;12(2):147-9. doi: 10.3109/00207458108985797.
The hypothermic effect of d-amphetamine was investigated in rats in which vasoconstriction or vasodilation was induced by pharmacological agents: aramine as vasoconstrictor and neprasol as vasodilator. The d-amphetamine-induced hypothermia was enhanced by both drugs among rats kept at 4 degrees C, and both drugs were unable to modify the d-amphetamine-induced hypothermia. These results indicate that although vasoconstriction and vasodilation play a major role in thermoregulation, d-amphetamine-induced hypothermia is not mediated peripherally by vasoconstriction. Since changes in basal metabolic rate, motor activity, food intake and vasoconstriction are not the peripheral mechanisms by which d-amphetamine induced hypothermia, the mechanisms is still unknown.
研究了在通过药物诱导血管收缩或血管舒张的大鼠中，右旋苯丙胺的低温效应：用阿拉明作为血管收缩剂，用奈哌索尔作为血管舒张剂。在4摄氏度饲养的大鼠中，这两种药物均增强了右旋苯丙胺诱导的体温过低，且这两种药物均无法改变右旋苯丙胺诱导的体温过低。这些结果表明，尽管血管收缩和血管舒张在体温调节中起主要作用，但右旋苯丙胺诱导的体温过低并非由血管收缩在外周介导。由于基础代谢率、运动活动、食物摄入量和血管收缩的变化不是右旋苯丙胺诱导体温过低的外周机制，因此该机制仍然未知。
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