Mello N K, Mendelson J H, King N W, Bree M P, Skupny A, Ellingboe J
Alcohol and Drug Abuse Research Center, McLean Hospital-Harvard Medical School, Belmont, Massachusetts 02178.
J Stud Alcohol. 1988 Nov;49(6):551-60. doi: 10.15288/jsa.1988.49.551.
Chronic alcohol dependence produces persistent amenorrhea in alcoholic women and female Macaque monkeys but the mechanism is unknown. In one amenorrheic alcohol-dependent monkey, prolactin levels increased from 16.5 to 63 ng/ml during chronic, high-dose alcohol self-administration (3.4 g/kg/day) and immunocytochemical examination of the anterior pituitary showed apparent hyperplasia of the lactotrophs. These data suggested that hyperprolactinemia might contribute to alcohol-induced amenorrhea. Four amenorrheic cycles (85-194 days) from two other alcoholic female monkeys that self-administered an average of 2.97 to 4.4 g/kg/day of alcohol were also studied. Each monkey became amenorrheic during the first menstrual cycle that alcohol was available. One monkey developed galactorrhea during a 97-day amenorrheic cycle when alcohol self-administration averaged 3.35 g/kg/day. Although prolactin levels were intermittently elevated above 20 ng/ml, average levels during these amenorrheic cycles (14.7 +/- 1.8 to 19.6 +/- 1.5 ng/ml) did not differ significantly from prolactin levels during normal ovulatory menstrual cycles when no alcohol was available (19.7 +/- 0.36 ng/ml). There was a negative correlation between daily alcohol dose and prolactin levels (p less than .01). High-dose alcohol self-administration was often associated with low normal prolactin levels, but a relative fall in alcohol dose was usually associated with elevated prolactin levels. These data suggest that both alcohol intoxication and relative alcohol withdrawal may alter basal prolactin levels. LH levels were significantly lower during amenorrheic cycles (16.9 +/- 1.2 to 24 +/- 1.4 ng/ml) than during nonalcohol control cycles (28 +/- 1.2 to 30 +/- 2.2 ng/ml) (p less than .001). These data are consistent with clinical data that suggest that hypothalamic amenorrhea is associated with suppression of gonadotropin secretory activity.
慢性酒精依赖会导致酗酒女性和雌性猕猴出现持续性闭经,但其机制尚不清楚。在一只闭经的酒精依赖猕猴中,在慢性高剂量酒精自我给药(3.4克/千克/天)期间,催乳素水平从16.5纳克/毫升升至63纳克/毫升,对垂体前叶的免疫细胞化学检查显示催乳细胞明显增生。这些数据表明高催乳素血症可能与酒精诱导的闭经有关。还研究了另外两只平均每天自我给药2.97至4.4克/千克酒精的酗酒雌性猕猴的四个闭经周期(85 - 194天)。每只猕猴在有酒精可获取的第一个月经周期就出现了闭经。一只猕猴在一个97天的闭经周期中出现了溢乳,此时酒精自我给药平均为3.35克/千克/天。尽管催乳素水平间歇性升高超过20纳克/毫升,但这些闭经周期中的平均水平(14.7±1.8至19.6±1.5纳克/毫升)与无酒精时正常排卵月经周期中的催乳素水平(19.7±0.36纳克/毫升)相比,差异无统计学意义。每日酒精剂量与催乳素水平之间存在负相关(p<0.01)。高剂量酒精自我给药常与低正常催乳素水平相关,但酒精剂量相对下降通常与催乳素水平升高相关。这些数据表明酒精中毒和相对戒酒都可能改变基础催乳素水平。闭经周期中的促黄体生成素(LH)水平(16.9±1.2至24±1.4纳克/毫升)显著低于无酒精对照周期(28±1.2至30±2.2纳克/毫升)(p<0.001)。这些数据与临床数据一致,临床数据表明下丘脑性闭经与促性腺激素分泌活动受抑制有关。