William W. Hurd
University of Alabama School of Medicine, United States of AmericaPresentation Title:
A Biomechanical Hypothesis for Labor Onset and Progression: Myometrial Shortening Stimulates Contractility
Abstract
The exact mechanisms that initiate
and drive the onset and progression of labor remain unclear. Throughout
pregnancy, myometrial contractility gradually intensifies due to a combination
of intracellular and hormonal factors, and these changes are proposed to be
responsible for the onset of labor. Simultaneously, the cervix undergoes a
gradual process of effacement and dilation, and these signs of cervical
ripening are the only physiological indicators predictive of labor onset. It is
plausible that an interaction between increasing uterine contractions and
cervical ripening plays a key role in triggering and sustaining labor. The essence of the biomechanical hypothesis presented
here is that labor is initiated and regulated by a positive feedback loop
involving uterine contractions, myometrial shortening, and the release of
prostaglandin F2α by the myometrium. Prostaglandin release is increased whenever
contractile force of surpasses resistance to myometrial shortening. Just before
and during early labor, cervical effacement and then dilation permit the cervix
to retract over the presenting fetal part. This mechanical process allows the
myometrium to make up a smaller portion of the uterine circumference, enabling
it to shorten during each contraction. Following full cervical dilation,
continued myometrial shortening results from reduction of uterine volume as the
fetus exits the uterus, culminating in full uterine emptying at delivery.
Because contractile forces can induce myometrial shortening—and this
shortening, in turn, enhances prostaglandin F2α release—the process forms a
reinforcing feedback loop essential to both the initiation and progression of
labor. When this loop is activated prematurely, due to either abnormally increased
contractile forces or decreased resistance to shortening, preterm labor may
result. The details of this
biomechanical hypothesis will be presented, followed by a review of the
laboratory and clinical evidence that either supports or contradicts this
hypothesis.
Biography
Dr. Hurd is Professor of Obstetrics and
Gynecology at the University of Alabama School of Medicine and Professor
Emeritus of Obstetrics and Gynecology at Duke University. Dr. Hurd maintained a nationally funded basic science
laboratory for more than two decades studying the physiology of myometrial
contractility. He has published
over 200 scholarly articles and book chapters, and is the co-editor of the
textbook, Clinical Reproductive Medicine
and Surgery, now in its 4th edition. He has served as president
of the Society of Reproductive Surgeons and the Council for Gynecologic
Excellence, as well as Chief Medical
Officer of the American Society for Reproductive Medicine.
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