Myometrial Shortening Stimulates Contractility: A Biomechanical Hypothesis for Labor Onset and Progression.

Abstract

The mechanisms responsible for the onset and progression of labor remain uncertain. Myometrial contractile activity gradually increases until labor onset as a result of a number of intrinsic and hormonal changes, and this a believed to be the essential process responsible for labor. At the same time, the cervix slowly effaces and dilates throughout pregnancy, and these are the only physiologic parameters predictive labor onset. It is feasible that an interaction exists between increasing contractile activity and cervical softening that is responsible for labor onset and progression. The novel biomedical hypothesis presented here is that labor onset and progression rely on a positive feedback loop involving uterine contractility, myometrial shortening, and shortening-related myometrial prostaglandin F_2α production, which occurs when contractile force exceeds the resistance to myometrial shortening. Immediately before labor onset and during early labor, first cervical effacement and then dilation allows the cervix to be pulled up over the presenting part, thus permitting myometrium to assume a decreasing percentage of uterine circumference, which enables myometrium to shorten with each uterine contraction. After complete dilation, further shortening is allowed by decreasing uterine volume resulting from fetal egress from the uterus and complete uterine emptying at delivery. Since contractile activity can shorten myometrium and shortening has been shown to increase myometrial prostaglandin F_2α production, the ability of myometrial shortening to stimulate contractile activity results in a positive feedback loop that plays an important role in both labor onset and progression. Premature labor occurs whenever this positive feedback loop develops prior to term because of pathologically increased contractile activity or decreased resistance to shortening. Details of this hypothesis and the mechanisms that either resist or allow myometrial shortening are presented, followed by a review of the laboratory and clinical evidence that either supports or appears to contradict this hypothesis.