Potter D A, Luther M F, Eddy C A, Siler-Khodr T M, King T S, Schenken R S
Department of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio 78284-7836, USA.
J Soc Gynecol Investig. 1999 Mar-Apr;6(2):88-94. doi: 10.1016/s1071-5576(98)00054-9.
To evaluate the effects of daily low-dose follicular-phase cocaine administration on menstrual cyclicity, ovulation rates, corpus luteum function, and hormone levels in rhesus monkeys.
Normally cycling, drug-naive, adult rhesus monkeys were randomized to receive either 1 mg/kg of cocaine (n = 7), 2 mg/kg of cocaine (n = 7), or normal saline (n = 7) daily on cycle days 2 to 14. Daily blood samples were obtained through indwelling catheters for measurement of serum gonadotropins and ovarian steroids. Daily vaginal swabs were obtained to determine onset of menses. Laparoscopy was performed 2 days after the midcycle estrogen peak to document ovulation. Daily caloric intakes as well as pretreatment and posttreatment weights were recorded.
Two of seven monkeys receiving 1 mg/kg per day and two of seven monkeys receiving 2 mg/kg per day of cocaine had timely ovulation and normal menstrual cycle lengths. One monkey receiving the 2-mg/kg dose ovulated on cycle day 24 and had a short luteal phase (7 days) with a mean progesterone level of 2.4 ng/mL. All seven saline-treated control monkeys ovulated normally; the mean cycle length was 29 days and all had adequate luteal phases. The difference in ovulation rates between cocaine-treated and control monkeys was statistically significant (P = .003). There were no differences in basal levels of LH or FSH between treatment groups. There were no significant differences in weight change or caloric intake among groups. One third of the subsequent menstrual cycles in cocaine-treated monkeys were of abnormal duration.
Daily low-dose follicular-phase cocaine administration disrupts menstrual cyclicity and folliculogenesis. This effect is independent of weight loss, caloric intake, and basal gonadotropin levels. Cocaine exposure may have a persistent effect on menstrual and ovarian cyclicity in some monkeys.
评估恒河猴在卵泡期每日给予低剂量可卡因对月经周期、排卵率、黄体功能及激素水平的影响。
将正常月经周期、未接触过药物的成年恒河猴随机分为三组，于月经周期的第2至14天，分别每日给予1mg/kg可卡因（n = 7）、2mg/kg可卡因（n = 7）或生理盐水（n = 7）。通过留置导管每日采集血样，测定血清促性腺激素和卵巢甾体激素水平。每日采集阴道拭子以确定月经来潮时间。在月经周期中期雌激素高峰后2天进行腹腔镜检查，记录排卵情况。记录每日热量摄入以及治疗前和治疗后的体重。
每日接受1mg/kg可卡因的7只猴子中有2只、每日接受2mg/kg可卡因的7只猴子中有2只排卵正常且月经周期长度正常。一只接受2mg/kg剂量的猴子在周期第24天排卵，黄体期较短（7天），平均孕酮水平为2.4ng/mL。所有7只接受生理盐水治疗的对照猴子排卵正常；平均周期长度为29天，黄体期均正常。可卡因治疗组和对照组猴子的排卵率差异具有统计学意义（P = .003）。各治疗组间促黄体生成素（LH）或促卵泡生成素（FSH）的基础水平无差异。各组间体重变化和热量摄入无显著差异。可卡因治疗组后续三分之一的月经周期持续时间异常。
卵泡期每日给予低剂量可卡因会扰乱月经周期和卵泡生成。这种影响与体重减轻、热量摄入及基础促性腺激素水平无关。可卡因暴露可能会对部分猴子的月经和卵巢周期产生持续影响。
