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醉酒期间,体温会影响乙醇敏感性的基因决定差异。

Genetically determined differences in ethanol sensitivity influenced by body temperature during intoxication.

作者信息

Alkana R L, Finn D A, Bejanian M, Crabbe J C

机构信息

Institute for Toxicology, School of Pharmacy, University of Southern California, Los Angeles 90033.

出版信息

Life Sci. 1988;43(24):1973-82. doi: 10.1016/0024-3205(88)90570-x.

Abstract

The present study investigated the importance of body temperature during intoxication in mediating differences between five inbred strains of mice (C57BL/6J; BALB/cJ; DBA/2J; A/HeJ; 129/J) in their acute sensitivity to the hypnotic effects of ethanol. Mice exposed to 22 degrees C after ethanol injection became hypothermic and exhibited statistically significant differences between strains in rectal temperatures at the return of the righting reflex (RORR), duration of loss of the righting reflex (LORR), and blood and brain ethanol concentrations at RORR. Exposure to 34 degrees C after injection offset ethanol-hypothermia and markedly reduced strain-related differences in rectal temperatures and blood and brain ethanol concentrations at RORR. Brain ethanol concentrations at RORR were significantly lower in C57, BALB, DBA and A/He mice exposed to 34 degrees C compared to mice exposed to 22 degrees C during intoxication suggesting that offsetting hypothermia increased ethanol sensitivity in these strains. Taken with previous in vitro studies, these results suggest that genetically determined differences in acute sensitivity to the behavioral effects of ethanol reflect differences in body temperature during intoxication as well as differences in sensitivity to the initial actions of ethanol at the cellular level.

摘要

本研究调查了中毒期间体温在介导五种近交系小鼠(C57BL/6J;BALB/cJ;DBA/2J;A/HeJ;129/J)对乙醇催眠作用的急性敏感性差异方面的重要性。乙醇注射后暴露于22摄氏度的小鼠体温过低,并且在翻正反射恢复(RORR)时的直肠温度、翻正反射消失持续时间(LORR)以及RORR时的血液和脑乙醇浓度方面,各品系间存在统计学上的显著差异。注射后暴露于34摄氏度可抵消乙醇诱导的体温过低,并显著降低RORR时直肠温度以及血液和脑乙醇浓度方面的品系相关差异。与在22摄氏度中毒期间暴露的小鼠相比,在34摄氏度暴露的C57、BALB、DBA和A/He小鼠在RORR时的脑乙醇浓度显著更低,这表明抵消体温过低会增加这些品系对乙醇的敏感性。结合先前的体外研究,这些结果表明,对乙醇行为效应的急性敏感性的遗传决定差异反映了中毒期间体温的差异以及细胞水平上对乙醇初始作用的敏感性差异。

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