![]() Fetal dehydroepiandrostenedione is converted in the placenta to estradiol and estriol. Rather, in humans, evidence suggests that placental production of corticotropin-releasing hormone (CRH) near term activates the fetal hypothalamic-pituitary axis and results in increased production of dehydroepiandrostenedione by the fetal adrenal gland. In contrast, humans lack placental 17α-hydroxylase, maternal and fetal levels of progesterone remain elevated, and no trigger exists for parturition because of an increase in fetal cortisol near term. If this increase in fetal ACTH and cortisol is blocked, progesterone levels remain unchanged, and parturition is delayed. ![]() The change in the circulating progesterone/estradiol concentration stimulates placental production of oxytocin and PG, particularly PGF 2α, which in turn promotes myometrial contractility. Fetal cortisol increases production of estradiol and decreases production of progesterone by a shift in placental metabolism of cortisol dependent on placental 17α-hydroxylase. In sheep, term labor is initiated through activation of the fetal hypothalamic-pituitary-adrenal (HPA) axis, with a resultant increase in fetal adrenocorticotropic hormone (ACTH) and cortisol. The fetus has a central role in the initiation of term labor in nonhuman mammals in humans, the fetal role is not completely understood ( Fig. The first three phases of labor require endocrine, paracrine, and autocrine interaction between the fetus, membranes, placenta, and mother. The final phase, uterine involution, occurs after delivery and is mediated primarily by oxytocin. In the human, this process at term may be protracted, occurring over days to weeks. In essence, the activation phase readies the uterus for the subsequent stimulation phase, when uterotonics-particularly PGs and oxytocin-stimulate regular contractions. This increase in the gap junctions between myometrial cells facilitates effective contractions. During the activation phase, estrogen begins to facilitate expression of myometrial receptors for prostaglandins (PGs) and oxytocin, which results in ion channel activation and increased gap junctions. The first phase is quiescence, which represents that time in utero before labor begins, when uterine activity is suppressed by the action of progesterone, prostacyclin, relaxin, nitric oxide, parathyroid hormone–related peptide, and possibly other hormones. ![]() The four phases of labor from quiescence to involution are outlined in Figure 12-1. Labor initiation is species specific, and the mechanisms of human labor are unique. The physiology of labor initiation has not been completely elucidated, but the putative mechanisms have been well reviewed by Liao and colleagues. This chapter describes the physiology and normal characteristics of term labor and delivery. More specifically, labor requires regular, effective contractions that lead to dilation and effacement of the cervix. Labor is defined as the process by which the fetus is expelled from the uterus. Factors that affect the average duration of the first and second stage of labor progress will be reviewed, and an evidence-based evaluation of strategies to support the mother during labor and facilitate safe delivery of the fetus will be presented. This chapter will review the characteristics and physiology of normal labor at term. ![]() The duration of the second stage of labor can be affected by a number of factors including epidural use, fetal position, fetal weight, ethnicity, and parity. The latent phase of labor is characterized by a slower rate of cervical dilation, whereas the active phase of labor is characterized by a faster rate of cervical dilation and does not begin for most women until the cervix is dilated 6 cm. These hormones upregulate transcription of progesterone, progesterone receptors, oxytocin receptors, and gap junction proteins within the uterus, which helps to facilitate regular uterine contractions. Although the exact trigger for human labor at term remains unknown, it is believed to involve conversion of fetal dehydroepiandrosterone sulfate (DHEAS) to estriol and estradiol by the placenta. The initiation of normal labor at term requires endocrine, paracrine, and autocrine signaling between the fetus, uterus, placenta, and the mother.
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