The process of luteolysis has been studied in immature rats in which superluteinization had been induced with pregnant mare serum gonadotropin (PMSG) and human chorionic gonadotrophin (HCG). Following prostaglandin F2α and the prostaglandin analogues, and at the end of the pseudopregnancy, the plasma levels of progesterone and 20α-dihydroprogesterone were measured and used as parameters of luteal function in relation to the capacity of the ovarian tissue to bind LH, FSH and prolactin (PRL) in vitro. On day 19 after HCG a marked decrease in the progesterone level from the day 8 level was observed concomitant with a marked increase in 20α-dihydroprogesterone. The capacity of the ovarian tissue to bind LH in vitro was markedly reduced on day 19 compared to day 8. Identical changes were observed 21 h after 1 mg prostaglandin F2α or prostaglandin analogues. Progesterone decreased from about 600 ng/ml to about 50 ng/ml, whereas the increase in 20α-dihydroprogesterone was from about 200 ng/ml to 500–1000 ng/ml and the reduction in LH binding sites was from 1.7 × 10−12 to 0.5 × 10−12 mol/mg protein. Nanogram amounts of the analogues were as effective as 1 mg of prostaglandin F2α. The number of FSH or PRL binding sites was not affected by spontaneous luteolysis or the treatment given.
By the use of graded doses of the prostaglandin analogues a negative correlation (r=−0.81) was found between plasma progesterone and 20α-dihydroprogesterone levels, and a positive correlation (r = 0.84) between LH binding sites and plasma progesterone levels.
The luteolysis induced by prostaglandin F2α or prostaglandin analogues was indistinguishable from the spontaneous luteolysis using these parameters.