Uterine contractility during pregnancy and the effect of abortifacient drugs.

There are a number of compounds in clinical use for termination of pregnancy. Treatment with all of them will result in increased uterine contractility. PGF2 alpha and PGE2 as well as different prostaglandin analogues all have a direct stimulatory effect on the myometrium, while other compounds such as hypertonic saline and Rivanol seem to act mainly through a stimulation of the endogenous production of PGF2 alpha. Treatment with antiprogestins which compete with progesterone at the receptor level or which inhibit progesterone biosynthesis results in an increased uterine contractility probably through a release from progesterone inhibition. If the withdrawal of progesterone also induces an increased endogenous prostaglandin production is unclear. The medical method to induce abortion which best resembles the physiological events during a spontaneous abortion is probably treatment with antiprogestins (receptor blockers or progesterone biosynthesis inhibitors) followed by prostaglandin.