Abstract

PIP: Aspirin and indomethacin have been found to be potent inhibitors of (PG) prostaglandin synthesis. Recent observations show that it is possible to partially reverse the block of ovulation caused by indomethacin if exogenous PGs, especially PGF2alpha are given at the same time as indomethacin. Indomethacin blockage of ovulation produces corpus lutea in which the eggs have been entrapped. The follicles proceed to luteinize and produce progesterone in amounts which do not differ from the normal. The differences between the effects seen on ovulation and the lack of effect seen on steroidogenesis may be a factor of timing. Recent evidence continues to support the view that PGF2alpha is the luteolysin in many of the nonprimate mammalian species. The same type of experiments in the monkey and human have produced completely different results. It is possible that very high levels are needed to accomplish luteolysis in primates. 1 similarity of results in studies of both primates and nonprimates is that when estrogens are administered, there follows a rapid luteal regression and a concomitant rise in PGFalpha. In the process of parturition, the role of PGs remains unsubstantiated. It is possible to speculate that PGF2alpha is responsible for increased uterine activity.