The physiological processes that regulate parturition-the bringing forth of young-and the onset of labor continue to be deined. Three general contemporaneous theories describe labor initiation. Viewed simplistically, the irst is the functional loss of prenancy maintenance actors. he second focuses on synthesis of actors that induce parturition. The third suggests that the mature fetus is the source of the initial signal or parturition commencement. Current research supports a model that draws from all three themes. However, labor onset clearly represents the culmination of a series of biochemical changes in the uterus and cervix. hese result from endocrine and paracrine signals emanating from both mother and fetus. Their relative contributions vary between species, and it is these diferences that complicate elucidation of the exact factors that regulate human parturition. When parturition is abnormal, then preterm-labor, dystocia, or postterm pregnancy may result. Of these, preterm labor remains the major contributor to neonatal mortality and morbidity.
The myometrial layer of the uterus is composed of bundles of smooth muscle cells surrounded by connective tissue. In contrast to skeletal or cardiac muscle, the smooth muscle cell is not terminally diferentiated and therefore is readily adaptable to environmental changes. Varied stimuli such as mechanical stretch, inlammation, and endocrine and paracrine signals can modulate
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FIGURE 21-1 The amnion synthesizes prostaglandins, and late in pregnancy, synthesis is augmented by increased phospholipase A2 and prostaglandin H synthase, type 2 (PGHS-2) activity. During pregnancy, the transport of prostaglandins from the amnion to maternal tissues is limited by expression of the inactivating enzymes, prostaglandin dehydrogenase (PGDH), in the chorion. During labor, PGDH levels decline, and amnion-derived prostaglandins can influence membrane rupture and uterine contractility. The role of decidual activation in parturition is unclear but may involve local progesterone metabolism and higher prostaglandin receptor concentrations, thus enhancing uterine prostaglandin actions and cytokine production. (Redrawn from Smith R: Parturition. N Engl J Med. 2007 Jan 18;356(3):271-283.) the transition of the smooth muscle cell among phenotypes that provide cell growth, proliferation, secretion, and contractility.
In addition to this phenotypic plasticity, several smooth muscle qualities confer advantages for uterine contraction eiciency and fetal delivery. First, the degree of smooth muscle cell shortening with contractions may be one order of magnitude greater than that attained in striated muscle cells. Second, forces can be exerted in smooth muscle cells in multiple directions. his difers from the contraction force generated by skeletal muscle, which is always aligned with the axis of the muscle fibers. hird, smooth muscle is not organized in the same manner as skeletal muscle. In myometrium, the thick and thin ilaments are found in long, random bundles throughout the cells. his plexiform arrangement aids greater shortening and force-generating capacity. Last, greater multidirectional force generation in the uterine fundus compared with that of the lower uterine segment permits versatility in expulsive force directionality.
Lining the thick muscular uterine walls, the endometrium is transformed by pregnancy hormones and is then termed decidua. Composed of stromal cells and maternal immune cells, the decidua serves to maintain the pregnancy via unique immuno regulatory functions that suppress inlammatory signals during gestation. However, at the end of pregnancy, decidual activation ensues. With this, the decidua transitions to induce inflammatory signals and withdraw active immunosuppression, which contribute to parturition initiation.