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To compare the circulating levels of bromocriptine after oral and vaginal administration of the drug.ExperimentalSeven ovulatory female volunteers and one hyperprolactinemic patient.Ovulatory volunteers were randomized to receive either oral or vaginal bromocriptine (2.5 mg). In a second session, the subjects were crossed-over to bromocriptine by the alternate route. An additional hyperprolactinemic patient received vaginal bromocriptine only.Serum bromocriptine and prolactin (PRL) levels were measured hourly for 12 hours in the normal volunteers and for 10 hours in the hyperprolactinemic patient.Circulating bromocriptine levels were significantly higher after vaginal bromocriptine after the 7th hour (P less than 0.05). The reduction in serum PRL was significantly greater after oral administration between 2 and 6 hours.Vaginally administered bromocriptine may result in a reduction in the overall dose required, thereby improving compliance without compromising therapeutic efficacy.

To determine if ovarian hyperandrogenism represents enhanced gonadotropic stimulation, augmented ovarian sensitivity to gonadotropins, or both, we have undertaken to evaluate (1) the 24-hour integrated concentrations of serum total testosterone (T) and luteinizing hormone (LH) and (2) the ovarian response of T to exogenous gonadotropic stimulation. To this end, two groups of women, hyperandrogenic anovulatory (n = 4) and early follicular phase (n = 4) normally-cycling controls, were subjected to continuous blood withdrawal over 24 hours with a portable Cormed pump (Cormed Inc., Middleport, NY) and to exogenous stimulation with human chorionic gonadotropin. Our current observations support the notion that ovarian hyperandrogenism represents the combined impact of an overall increase in gonadotropic support coupled with augmented ovarian sensitivity to gonadotropic stimulation.

Chronic and transient hyperprolactinemia have been associated with luteal phase dysfunction in both spontaneously cycling women and those subjected to ovarian hyperstimulation by exogenous gonadotropins. It is the objective of the in vitro and in vivo studies reported herein to examine the possibility that prolactin (PRL), a known constituent of ovarian follicular fluid, may account, at least in part, for the luteinization inhibitory (LI) activity exerted by follicular fluid (FF) under both physiologic and pathophysiologic circumstances. In vitro treatment with human PRL (100 ng/ml) reduced by 57% the specific binding of luteinizing hormone (LH) to follicle-stimulating hormone(FSH)-primed cultured rat granulosa cells, an effect associated with a 2.6-fold diminution of human chorionic gonadotropin (hCG; 10 ng/ml)-stimulated progesterone biosynthesis. Importantly, the ability of PRL to exert a direct inhibitory effect on FSH-supported LH binding was fully reproduced under in vivo conditions. Inasmuch as the acquisition of LH receptors and progesterone (P) biosynthetic capacity are acceptable as criteria of granulosa cell luteinization, the authors' findings indicate that PRL, acting at concentrations achievable in vivo within the ovarian FF, may account, if only in part, for physiologically encountered LI-like activity. Moreover, subject to limitations imposed by the rat model employed, consideration also must be given to the possibility that hyperprolactinemia-associated luteal phase dysfunction may not only reflect the suppressive effect(s) of PRL at the central level of the reproductive axis, but may also be due, at least in part, to the consequences of inappropriately elevated PRL at the level of the follicular microenvironment.