Acute effects of an antiserum to luteinizing hormone on ovarian steroidogenesis in the pregnant rat.

Pregnant rats were injected s.c. at 09.00 h on day 8 of pregnancy (day 1 = sperm-positive vaginal smear) with either 0.2 or 0.5 ml equine antiserum to bovine LH (anti-LH) while control rats were injected with 0.5 ml normal horse serum (NHS). Rats were decapitated 1, 3, 6, 24 and 48 h later and serum was saved for radioimmunoassay of progesterone, androstenedione, testosterone, oestrone and oestradiol. One ovary was kept for histology, and from the other, corpora lutea (three/animal) and the non-luteal ovary (ovarian remnant from which all corpora lutea were removed) were saved for steroid determinations. The production rate of steroids by the luteal and non-luteal ovarian compartment was assessed by incubation in Krebs--Ringer bicarbonate buffer for 2 h. A significant decrease in the serum concentrations of all steroid hormones was induced by 6 h after treatment with anti-LH; progesterone being the first hormone to be consistently reduced (by 3 h). The steroid concentrations remained lower than those in control rats on days 9 and 10. A single injection of anti-LH reduced the number of health antral follicles by 3 h but there were always two to four normal antral follicles per ovary on days 8-10. The initial hormonal changes in the non-luteal ovary after LH deprivation were decreases in the concentration and production rates of the androgens and oestrogens. The initial concentration of non-luteal progesterone was lower 3 and 6 h after anti-LH than in control rats. Although anti-LH induced a decrease in the serum concentration of progesterone 24 and 48 h later, the corpora lutea contained more progesterone on day 8 and produced in vitro more progesterone than controls on day 8 after 0.2 and 0.5 ml anti-LH and on day 9 when only 0.5 ml was give. The increase in the initial concentration of progesterone on day 8 probably represents accumulation resulting from inhibition of luteal progesterone release. It appears, therefore, that the initial alteration after LH deprivation is inhibition of the release of luteal progesterone and this alone is sufficient to account for the interruption of pregnancy. The in-vivo increase in luteal steroidogenesis following LH deprivation was observed to some extent with androstenedione bu testosterone was unaffected. Luteal aromatizing enzymes appeared to be very sensitive to LH deprivation on day 8 since the concentration and production of oestrogen decreased without concomitant decreases in androgen. Progesterone (4 mg) administered along with 0.2 ml anti-LH on day 8 prevented luteal regression and the corpora lutea synthesized progesterone and androgens similarly to NHS-treated controls; however, the corpora lutea of the progesterone-treated group contained and produced less oestrogen than controls.