William Hurd

University of Alabama School of Medicine, USA

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

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Biography

William 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. He 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. 

Abstract

The mechanisms responsible for initiation and sustainment of labor remain uncertain. Throughout pregnancy, uterine contractility increases secondary to changes in both cellular signaling pathways and hormonal stimulation. This gradual rise in uterine activity is believed to contribute to the onset of labor. At the same time, the cervix softens, shortens (effaces), and begins to dilate - a process known as cervical ripening. Currently, signs of cervical ripening are the only physical changes that have been found to predict labor onset. It seems likely that the coordination between increasing uterine contractions and cervical ripening plays a critical role in triggering and maintaining labor.  This novel biomechanical hypothesis proposes that labor begins and progresses as a result of a positive feedback loop involving uterine contractions, myometrial shortening, and increased release of prostaglandin F2? (PGF2?) from myometrium. This prostaglandin release continues as long as uterine contractions are strong enough to overcome resistance to myometrial shortening.  Just before labor onset and continuing throughout early labor, the cervix effaces and dilates, allowing it to retract over the fetal presenting part. These mechanical changes reduce the cervical contribution to the uterine circumference, enabling the myometrium to shorten with each contraction. After the cervix is fully dilated, continued myometrial shortening is allowed by reduction in uterine volume as the fetus exits the uterus, culminating in uterine emptying at delivery.  Because uterine contractions promote myometrial shortening and shortening further increases PGF2? production, a positive feedback loop results that is responsible for both the initiation and progression of labor. When this process starts prior to term, whether due to decreased cervical resistance or unusually strong contractions, preterm labor occurs. The presentation will delve deeper into the proposed biomechanical hypothesis and examine both laboratory and clinical findings that support or challenge its validity.