Glucocorticoid suppression of intraovarian levels of prostaglandins and plasminogen activator activity at ovulation in the rat ovary.

Aim: Ovulation is a local physiological inflammatory process with active participation of inflammatory mediators and immune cells. To prevent extensive inflammatory injury to the follicle at ovulation there is also a local anti-inflammatory system at ovulation, converting the inactive glucocorticoid cortisone to the more potent cortisol. The aim of this study was to examine the effects of the potent glucocorticoid analogue, dexamethasone (DEX), on ovulation rate and the ovarian production of the ovulatory mediators prostaglandins (PG) and plasminogen activators (PA).

Methods: DEX (0.3, 3, or 100 microM) was administered to an in vitro rat ovarian perfusion system prior to the addition of an ovulation-inducing dose of luteinizing hormone (LH) and 3-isobutyl-1-methylxanthine (IBMX). Control ovaries were perfused only with LH + IBMX. Each perfusion experiment extended over 20 h with ovulation occurring in vitro around 12-15 h after hormonal stimulation. In a second set of perfusion experiments, extending over 10 h, the tissue levels of PG and PA activity in the ovary were evaluated at a time 2-5 h before anticipated ovulation.

Results: The median numbers of ovulated oocytes in the groups with DEX of 0.3, 3, and 100 microM were 17.0, 8.5 and 11.0 per treated ovary, respectively. These numbers were not different from those of LH + IBMX-controls (12.5). DEX (100 microM) suppressed tissue levels of PGE(2) and PA activity and decreased (DEX 3 microM, 100 microM) estradiol levels in the perfusion media.

Conclusion: These results indicate that certain degrees of suppression of PG, PA activity, and estradiol are not sufficient to modulate ovulation rate and/or that glucocorticoids may positively modulate other mediator pathways that exert inhibitory influence on ovulation.