Complex Interplay Between Maternal and Fetal Factors Induces Parturition

The duration of pregnancy in women averages 270 ± 14 days from the time of fertilization. Parturition or the onset of birth is regulated by the interactions of fetal and maternal factors. Uncoordinated uterine contractions start about 1 month before the end of gestation. The termination of pregnancy is initiated by strong rhythmic contractions that may last several hours and eventually generate enough force to expel the conceptus. The contraction of the uterine muscle is regulated by hormones and by mechanical factors. The hormones include progesterone, estrogen, prostaglandins, oxytocin, and relaxin. The mechanical factors include distension of the uterine muscle and stretching or irritation of the cervix.

Progesterone hyperpolarizes myometrial cells, lowers their excitability, and suppresses uterine contractions. It also prevents the release of phospholipase A2, the rate-limiting enzyme in prostaglandin synthesis. Estrogen, in general, has the opposite effects. The maintenance of uterine quiescence throughout gestation, preventing premature delivery, is called the progesterone block. In many species, a sharp decline in the circulating levels of progesterone and a concomitant rise in estrogen precede birth. In humans, progesterone does not fall significantly before delivery. However, its effective concentration may be altered by a rise in placental progesterone-binding protein or by a decline in the number of myometrial progesterone receptors.

Prostaglandins F2A and E2 are potent stimulators of uterine contractions and also cause significant ripening of the cervix and its dilation. They increase intracellular calcium concentrations of myometrial cells and activate the actin-myosin contractile apparatus. Shortly before the onset of parturition, the concentration of prostaglandins in amniotic fluid rises abruptly. Prostaglandins are produced by the myometrium, decidua, and chorion. Aspirin and in-domethacin, inhibitors of prostaglandin synthesis, delay or prolong parturition.

Oxytocin is also a potent stimulator of uterine contractions, and its release from both maternal and fetal pitu-itaries increases during labor. Oxytocin is used clinically to

Indifferent stages

Genital fold Genital swelling

Genital tubercle

Glans

Fused urogenital folds Anus Urethral groove

Scrotum

Prepuce

Body of penis

Scrotal raphe

Genital fold Genital swelling

Genital tubercle

Fused Clit

0 Differentiation of the external genitalia from bipotential primordial structures.

Glans

Urethral groove Anus

Labia minora Labia majora

Clitoris

Urethral orifice Hymen

0 Differentiation of the external genitalia from bipotential primordial structures.

induce labor (see Clinical Focus Box 39.2). The functional significance of oxytocin is that it helps expel the fetus from the uterus, and by contracting uterine muscles, it reduces uterine bleeding when bleeding may be significant after delivery. Interestingly, oxytocin levels do not rise at the time of parturition.

Relaxin, a large polypeptide hormone produced by the corpus luteum and the decidua, assists parturition by softening the cervix, permitting the eventual passage of the fetus, and by increasing oxytocin receptors. However, the relative role of relaxin in parturition in humans is unclear, as its levels do not rise toward the end of gestation. Re-laxin reaches its peak during the first trimester, declines to about half, and remains unchanged throughout the remainder of pregnancy.

The fetus may play a role in initiating labor. In sheep, the concentration of ACTH and cortisol in the fetal plasma rise during the last 2 to 3 days of gestation. Ablation of the fetal lamb pituitary or removal of the adrenals prolongs gestation, while administration of ACTH or cortisol leads to premature delivery. Cortisol enhances the conversion of progesterone to estradiol, changing the progesterone-to-estrogen ratio, and increases the production of prostaglandins. The role of cortisol and ACTH, however, has not been established in humans. Anencephalic or adrenal-deficient fetuses, which lack a pituitary and have atrophied adrenal glands, have an unpredictable length of gestation. Those pregnancies also exhibit low estrogen levels because of the lack of adrenal an drogen precursors. Injections of ACTH and Cortisol in late pregnancy do not induce labor. Interestingly, the administration of estrogens to the cervix causes ripening, probably by increasing the secretion of prostaglandins.

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Responses

  • Monika
    What fetal and maternal factors start labor?
    8 years ago
  • Robur Chubb-Baggins
    How can labor be induced injection of estrogen?
    8 years ago

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