HUMAN MENOPAUSAL GONADOTROPIN HUMAN CHORIONIC GONADOTROPIN-INDUCED OVARIAN HYPERSTIMULATION WITH TRANSIENT HYPERPROLACTINEMIA - STEROIDOGENESIS ENHANCED DURING BROMOCRIPTINE THERAPY IN MONKEYS

To examine the role of gonadotropin-induced hyperprolactinemia on reproductive function, 17 euprolactinemic ovulatory monkeys were given extended fixed dose regimens of human menopausal gonadotropin (hMG) (12 days), followed by hCG [human chorionic gonadotropin] the next day, and some animals then received bromocriptine. All animals were given hMG/hCG from day 3 (D3) until D14, with hCG on D15; those in group I (n = 12) received no further therapy, while those in group II (n = 5) received bromocriptine (0.25 mg/kd .cntdot. day, i.m.) daily from the day of hCG administration until menses. Ovarian hyperstimulation developed to various degrees in all animals. Based on serum estradiol (E2) levels, 13 were high responders (E2, > 1000 pg/mg), 2 were medium responders (E2, 500-1000 pg/ml), and 2 were low responders (E2, 150-500 pg/ml). In group I, transient hyperprolactinemia occurred in the luteal phases in 8 of the 12 animals compared to the follicular phase levels in the same animals (P < 0.01). In group II, bromocriptine treatment in the luteal phase prevented hyperprolactinemia, but there was no change in the menstrual cycle or luteal phase lengths; however, significant luteal phase increase in progesterone (P < 0.005) and E2 (P < 0.02) secretion occurred during bromocriptine therapy. Deliberate hMG/hCG studies in euprolactinemic women seem indicated to learn whether women so treated experience estrogen-progesterone-induced hyperprolactinemia like that in monkeys and, if so, to determine its consequences on the reproductive process.