Effect of chronic intoxication and naloxone on the ethanol-induced increase in plasma corticosterone.

Effect of chronic intoxication and naloxone on the ethanol-induced increase in plasma corticosterone.
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慢性中毒和纳洛酮对乙醇引起的血浆皮质酮增加的影响。

DOI:
10.1016/0024-3205(81)90645-7
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发表时间:
1981
期刊:
影响因子:
6.1
通讯作者:
Joseph R. Prohaska
Joseph R. Prohaska
中科院分区:
医学2区
文献类型:
--
作者:
E. Knych;Joseph R. Prohaska

文献摘要

被引文献

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乙醇(0.5-4.0 g/kg)会导致清醒、未受干扰的雄性大鼠血浆皮质酮立即出现剂量依赖性升高。至少两天的慢性中毒导致对这种效应的耐受。慢性中毒还显着升高了这种类固醇的早晨谷值。纳洛酮(1 mg/kg)的联合给药可防止对乙醇的即时刺激作用产生耐受性,但不会改变皮质酮升高的谷值水平。 Naloxene (1 mg/kg) 不会改变乙醇对未接触过乙醇的动物皮质酮的刺激作用。这些数据表明,对乙醇引起的皮质酮升高的耐受性发展过程是由阿片受体介导的。乙醇刺激皮质酮分泌的能力的改变可能是未来乙醇耐受性发展研究的有用终点。
Ethanol (0.5–4.0 g/kg) induced an immediate, dose-dependent rise in plasma corticosterone in the conscious, undisturbed male rat. Chronic intoxication for at least two days resulted in tolerance to this effect. Chronic intoxication also significantly elevated the morning trough levels of this steroid. Co-administration of naloxone (1 mg/kg) prevented the development of tolerance to the immediate stimulatory effect of ethanol but did not alter the elevated trough levels of corticosterone. Naloxene (1 mg/kg) did not alter the stimulatory effect of ethanol on corticosterone in ethanol-naive animals. These data suggest that the process of tolerance development to the ethanol-induced rise in corticosterone is mediated by an opiate receptor. Alterations in the ability of ethanol to stimulate corticosterone secretion may be a useful endpoint for future studies of tolerance development to ethanol.