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  • Title: Uterine contractility during pregnancy and the effect of abortifacient drugs.
    Author: Bygdeman M, Swahn ML.
    Journal: Baillieres Clin Obstet Gynaecol; 1990 Jun; 4(2):249-61. PubMed ID: 2225598.
    Abstract:
    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. Factors regulating uterine activity during pregnancy and parturition or abortion, and pharmacological manipulation of uterine activity are the subject of this review. The uterus is normally quiescent during pregnancy. Prostaglandins (PGs) are regarded as intrinsic simulators of uterine contractility: endogenous PGs are correlated with initiating of labor, and considered the last step in the course of events leading to labor. Progesterone is regarded as a local regulator of uterine sensitivity to other oxytocics. OXytocin is not effective alone as a uterine stimulant until the uterus is already stimulated. It binds to receptors in the decidua which promote local PG synthesis. The natural PGs, PGF2alpha and PGE2 stimulate uterine tonus rapidly, eventually leading to onset of regular contractions if administration is continued. PG analogs used routinely in several countries are gemeprost (May & Baker, Dagenham, UK), carboprost (Upjohn, Kalamazoo, USA), and sulprostone (Schering, Berlin). There are more potent, more specific to the uterus rather than the gastrointestinal tract, and can be given by routes other than intravenous. Antiprogestins e.g., RU-486, and progesterone synthesis inhibitors e.g., epostane, act on the myometrium by converting it to a reactive or spontaneously active organ. These agents will terminate early pregnancy if given with PGs. Both hypertonic saline and Rivanol, long used as 2nd trimester abortifacients, act by initiating decidual regression and PG release.
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