Cañez M S, Samuels M H, Luther M F, King T S, Schenken R S
Department of Obstetrics and Gynecology, University of Texas Health Science Center, San Antonio 78284-7836.
Am J Obstet Gynecol. 1992 Dec;167(6):1785-93. doi: 10.1016/0002-9378(92)91776-7.
Our objective was to determine whether cocaine alters gonadotropin secretion in oophorectomized monkeys.
Oophorectomized monkeys with elevated gonadotropin levels were chronically cannulated to allow blood sampling every 15 minutes. Monkeys received either saline solution or 2 or 4 mg/kg cocaine hydrochloride as an intravenous bolus. Other oophorectomized monkeys were pretreated with either saline solution or 4 mg/kg cocaine 2 hours before bolus gonadotropin-releasing hormone administration, and plasma luteinizing hormone and follicle-stimulating hormone levels were measured every 15 minutes for 3 hours. Monkeys were also given either saline solution or 4 mg/kg of cocaine with gonadotropin-releasing hormone simultaneously, and plasma gonadotropin levels were measured every 15 minutes for 3 hours. Serum luteinizing hormone and follicle-stimulating hormone levels were measured by radioimmunoassay.
Both doses of cocaine resulted in a significant decrease in luteinizing hormone levels compared with controls. Follicle-stimulating hormone levels were significantly decreased only with the 4 mg/kg dose of cocaine. There was no difference in luteinizing hormone and follicle-stimulating hormone responses to gonadotropin-releasing hormone in the cocaine-treated monkeys compared with saline solution-treated monkeys by using repeated-measures analysis of variance.
These findings demonstrate that acute cocaine administration to oophorectomized primates inhibits basal luteinizing hormone-follicle-stimulating hormone secretion but not gonadotropin-releasing hormone-stimulated luteinizing hormone and follicle-stimulating hormone release. In the absence of an effect on gonadotropin-releasing hormone-stimulated gonadotropin release, we conclude that the impaired luteinizing hormone-follicle-stimulating hormone secretion after cocaine administration is due in part to a direct effect of cocaine on gonadotropin-releasing hormone neurons or on hypothalamic neurotransmitter modulation of gonadotropin-releasing hormone release.
我们的目的是确定可卡因是否会改变去卵巢猴子的促性腺激素分泌。
对促性腺激素水平升高的去卵巢猴子进行长期插管，以便每15分钟采集一次血液样本。猴子接受生理盐水或2或4mg/kg盐酸可卡因静脉推注。其他去卵巢猴子在推注促性腺激素释放激素前2小时用生理盐水或4mg/kg可卡因预处理，然后每15分钟测量一次血浆黄体生成素和促卵泡激素水平，持续3小时。猴子还同时接受生理盐水或4mg/kg可卡因与促性腺激素释放激素，每15分钟测量一次血浆促性腺激素水平，持续3小时。通过放射免疫测定法测量血清黄体生成素和促卵泡激素水平。
与对照组相比，两种剂量的可卡因均导致黄体生成素水平显著降低。仅4mg/kg剂量的可卡因使促卵泡激素水平显著降低。通过重复测量方差分析，与生理盐水处理的猴子相比，可卡因处理的猴子对促性腺激素释放激素的黄体生成素和促卵泡激素反应没有差异。
这些发现表明，对去卵巢灵长类动物急性给予可卡因会抑制基础黄体生成素-促卵泡激素分泌，但不会抑制促性腺激素释放激素刺激的黄体生成素和促卵泡激素释放。由于对促性腺激素释放激素刺激的促性腺激素释放没有影响，我们得出结论，可卡因给药后黄体生成素-促卵泡激素分泌受损部分归因于可卡因对促性腺激素释放激素神经元的直接作用或对促性腺激素释放激素释放的下丘脑神经递质调节的直接作用。
