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本实验使用家兔诱导排卵动物模型,分别观察了消旋18-甲基炔诺酮和左旋18-甲基炔诺酮对于用铜盐、由PMSG和hCG以及由LH-RH诱导的家兔排卵的影响。实验分三组:一组于实验第1～3天皮下注射雌二醇(每只100μg/天),第4天经耳缘静脉注射1%醋酸酮(0.4ml/kg),24小时后处死并检查排卵点。二组于实验第1～2天皮下注射雌二醇,第4天皮下注射一次LH-RH(12.5μg/只),48小时后处死并观察和记数排卵点。三组于实验第2天皮下注射PMSG(12.5u),第4天经耳缘静脉注射50iuhCG,48小时后处死并检查排卵点。各组中的实验组于第1～4天肌肉注射消旋18-甲基炔诺酮或左旋18-甲基炔诺酮(每只8mg/天)对照组给予等量溶媒。结果表明,两种18-甲基炔诺酮皆明显抑制由铜盐诱导的家兔排卵,抗排卵率分别为83.3%和66.7%。然而,两者对于由LH-RH和由PMSG与hCG诱导的家兔排卵皆无明显影响。以上结果提示,消旋18-甲基炔诺酮和左旋18-甲基炔诺酮的抗排卵作用可能是通过干扰下丘脑LH-RH的释放而实现的,并非由于在垂体水平拮抗LH-RH的作用或在性腺水平上拮抗促性腺激素作用的结果。
In this experiment, rabbit ovulation induction animal models were used to observe the effects of racemic 18-norgestrel and levonorgestrel on ovulation induced by copper salts, PMSG and hCG, and LH-RH induced rabbits respectively Impact. The experiment was divided into three groups: one group received subcutaneous injection of estradiol (100 μg / day) on days 1 to 3 of the experiment, and 1% acetic anhydride (0.4 ml / kg) And check ovulation point. The two groups were injected with estradiol subcutaneously on the first to the second day of experiment, LH-RH (12.5μg / one) was injected subcutaneously on the fourth day and sacrificed 48 hours later and the ovulation point was observed and counted. Three groups were injected with PMSG (12.5u) subcutaneously on the second day of the experiment, and 50iuhCG was injected through the ear marginal vein on the fourth day. After 48 hours, the ovulation sites were sacrificed. The experimental groups in each group were administered an equal volume of vehicle with intramuscular injection of racemic 18-norgestrel or levonorgestrel (8 mg / day each) on day 1 to 4. The results showed that both 18-norgestrel and 18-norgestrel significantly inhibited the copper-induced ovulation in rabbits, the anti-ovulation rate was 83.3% and 66.7%. However, both had no significant effect on ovulation in rabbits induced by LH-RH and by PMSG and hCG. The above results suggest that the anti-ovulation effect of racemic 18-norgestrel and levonorgestrel may be achieved by interfering with the hypothalamic LH-RH release, not by antagonizing LH-RH at the pituitary level Or at the gonadal level as a result of antagonizing the effects of gonadotropins.