Abstract

PIP: This literature review, which describes the structure of myometrial muscle and the regulation of its contractility, cites research from 1971 to 1989. The functions of the myometrium and the cervix are interrelated and coordinated during pregnancy and labor. The structure of smooth muscle, by allowing contraction in any direction, permits the uterus to assume the shape and size necessary to accommodate the fetus. Myometrial smooth muscle cells communicate via gap junctions, which synchronize myometrial function via conduction of electrophysiological stimuli during labor. These junctions increase in number prior to labor. This is regulated by estrogen, progesterone, and prostaglandins (PGs). The structures of myosin and actin and their movement during contraction are described. Estrogen, via alpha adrenergic receptors, causes a decrease in cAMP levels. It also increases the number of oxytocin receptors. Progesterone, via beta adrenergic receptors, causes an increase in cAMP levels. While estrogen leads to increased production of PGF2alpha, progesterone stimulates the production of prostacyclin synthase, Mifepristone, which blocks progesterone at the receptor level, increases uterine activity and sensitivity to PG. Human amnion and chorion produce mainly PGE2. The decidua produces PGE2 and PGF2alpha. Prostaglandins induce uterine activity at all stages of gestation when they are administered exogenously. Their production by uterine tissues increases during pregnancy, as does their concentration in amniotic fluid and in maternal blood and urine. Their roles in labor, whether natural or induced, include the softening of the cervix, the induction of gap junctions, and the direct stimulation of myometrial contractions. Although PGE2 and PGF2alpha relax cervical smooth muscle, they contract the myometrium by acting as calcium ionophpores. The production of PGE2, PGF2alpha, and other eicosanoids by the fetoplacental production of PGE2, PGF2alpha, and other eicosanoids by the fetoplacental unit is related to increased contractile activity during labor. What is produced in the eiconsanoid pathway changes dynamically with the phases of the reproductive cycle and the local concentrations of enzymes. Because of the rise in arachidonic acid in amniotic fluid during labor, fetal membranes may be involved with the initiation of regular uterine contractions. In addition, any stimulus facilitating PGE2 synthesis in the fetal membrane (hypoxia, infection, exposure to oxytocin, hypertonic solutions, prostaglandins, or arachidonic acid) would induce the same series of steps leading to formation of PGF2alpha in the decidua and the myometrium. Since natural prostaglandins are rapidly metabolized, and induction of abortion requires a longer presence, analogues have been developed for this use. These include gemeprost, sulprostone, and minprostin. Their action is more prolonged and specific to uterine tissue than their parent compounds.