ALCOHOL EFFECTS ON NALOXONE-STIMULATED LUTEINIZING-HORMONE, PROLACTIN AND ESTRADIOL IN WOMEN
ALCOHOL EFFECTS ON NALOXONE-STIMULATED LUTEINIZING-HORMONE, PROLACTIN AND ESTRADIOL IN WOMEN
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DOI：
10.15288/jsa.1987.48.287
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发表时间：
1987-07-01
期刊：
影响因子：
--
通讯作者：
SCHIFF, I
中科院分区：
文献类型：
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作者：
MENDELSON, JH;MELLO, NK;SCHIFF, I
血浆促黄体生成素（LH），雌二醇，催乳素和孕酮水平在9个正常的成年女性之前和之后的纳洛酮和口服摄入乙醇或安慰剂对照溶液进行了测量。在月经周期的黄体中期进行的双盲研究中，每个受试者都作为自己的对照。平均值（.+-. SD）孕酮水平为13.9 ±-。1.3在对照条件下和13.9 . ±. 1.7在酒精条件下。平均峰值血液酒精含量为100 ± 100。开始饮酒后45-60分钟内13 mg/dl。在安慰剂对照条件下，纳洛酮刺激血浆LH和催乳素显著增加，但未增加雌二醇或孕酮。酒精并没有减弱显着的纳洛酮刺激LH，孕酮水平在酒精和对照条件下是相等的。酒精显着增强纳洛酮刺激催乳素和雌二醇。酒精给药显著增强纳洛酮诱导的血浆催乳素水平升高。酒精给药后，纳洛酮还诱导血浆雌二醇水平显著升高，并在整个180分钟采样期间持续升高。酒精增强纳洛酮刺激的催乳素和雌二醇的机制仍有待确定。纳洛酮刺激的催乳素分泌的酒精相关增加可能反映了纳洛酮内源性阿片类药物阻断后下丘脑和/或垂体对酒精的敏感性增加或雌激素水平升高的影响。纳洛酮和酒精同时给药后血浆雌二醇水平显著升高可能是肝内乙醇催化剂相关类固醇生物转化改变的结果。
Plasma luteinizing hormone (LH), estradiol, prolactin and progesterone levels were measured in nine normal adult women prior to and following administration of naloxone and oral ingestion of ethanol or placebo-control solution. Each subject served as her own control in a double-blind study carried out during the midluteal phase of the menstrual cycle. The mean (.+-. SD) progesterone level was 13.9 .+-. 1.3 during control conditions and 13.9 .+-. 1.7 during alcohol conditions. The mean peak blood alcohol level was 100 .+-. 13 mg/dl within 45-60 min after initiation of drinking. Under placebo-control conditions, naloxone stimulated a significant increase in plasma LH and prolactin but did not increase estradiol or progesterone. Alcohol did not attenuate the significant naloxone stimulation of LH, and progesterone levels were equivalent under alcohol and control conditions. Alcohol significantly enhanced naloxone stimulation of prolactin and estradiol. Alcohol administration significantly augmented the naloxone-induced increase in plasma prolactin levels. After alcohol administration, naloxone also induced a significant increase in plasma estradiol levels, which was sustained throughout the 180-min sampling period. The mechanism underlying alcohol''s enhancement of naloxone-stimulated prolactin and estradiol remain to be determined. The alcohol-related increase in naloxone-stimulated prolactin secretion may reflect increased hypothalamic and/or pituitary sensitivy to alcohol following endogenous opioid blockade by naloxone or an effect of increased estrogen levels. The significant increase in plasma estradiol levels following concurrent naloxone and alcohol administration may occur as a consequence of alterations in steroid biotransformation associated with intrahepatic ethanol catabolism.