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Fertilization, Pregnancy And Parturition


Fertilization, Pregnancy And Parturition
Fertilization
The unfertilized ovum can survive for up to 24 h after ovulation, and sperm remain viable in the uterus for up to 5 days after ejaculation. The environment of the female tract triggers the capacitation of sperm. This is a prerequisite for fertilization that involves remodelling of the lipids and glycoproteins of the sperm plasma membrane, coupled with increased metabolism and motility. The ovum is surrounded by the zona pellucida, an acellular membrane bearing the glycoprotein ZP3 that acts as a sperm receptor. Fertilization occurs in the oviduct, when a single capacitated sperm binds to ZP3 and under-goes the acrosome reaction. The acrosome is a body containing proteolytic enzymes that is attached to the sperm head (Fig. 52a). When a sperm binds to ZP3, the acrosomal enzymes are released to digest a pathway for the sperm to penetrate the ovum, within which the contents of the sperm head, including its genetic material, are deposited. This event leads to a chain of reactions that denies access to further sperm penetration. The ovum first undergoes electrical depolarization and then discharges granules that impair further sperm binding at the zona pellucida (the cortical reaction). In this way, fertilization is normally restricted to one sperm per ovum. Some 2–3 h after penetrating the ovum, the sperm head forms the male pronucleus which joins with the female pronucleus from the ovum (Fig. 52a). Fusion of the pronuclei combines the parental genetic material from the gametes to form the zygote.


Fertilization, Pregnancy And Parturition

Pregnancy
The zygote is propelled by cilia and muscular contractions of the Fal-lopian tube into the uterus, where it implants in the endometrium. During this journey, the zygote undergoes a number of cell divisions to form the morula, a solid ball of 16 cells that ‘hatches’ from the zona pellucida and develops into the blastocyst, in which embryonic cells are surrounded by trophoblasts (Fig. 52a). The trophoblasts are responsible for implantation, digesting away the uterine endometrial wall to form a space for the embryo, opening up a pathway to the maternal circulation (via the spiral arteries of the uterus) and forming the fetal portion of the placenta. The tissue engineering activities of trophoblasts are mediated by epidermal growth factor (EGF) (Chapter 46) and interleukin-1β. Implantation is complete within 7–10 days of fertilization, at which time the embryo and early placenta begin to secrete human chorionic gonadotrophin (hCG). The appearance of hCG in the plasma and urine is one of the earliest signs of successful conception, and its detection forms the basis of pregnancy testing kits. hCG is a glycoprotein similar to LH that stimulates progesterone secretion from the corpus luteum. Progesterone levels rise steadily throughout pregnancy and fall sharply at term (Fig. 52b). This steroid ensures that the smooth muscle of the uterus remains quiescent during gestation (essential for a successful pregnancy), stimulates mammary gland development and prepares the maternal brain for motherhood. The  placenta  also  secretes  chorionic  somatomammotrophin,  a growth hormone-like protein that mobilizes metabolic fuels (Chapter 43) and promotes mammary gland growth, and oestrogen (mainly oestriol) that stimulates uterine expansion to accommodate the growing fetus. Fetal development occurs within a fluid-filled sac, known as the amniotic membrane, which provides a protective buffer against physical trauma. Pregnancy makes many physiological demands on the mother. The ventilation rate, cardiac output and plasma volume increase to supply fetal–maternal oxygen and water demands; the gastrointestinal absorption of minerals is enhanced; and the renal glomerular filtration rate (Chapter 32) rises to cope with fetal waste production.

Parturition
After some 40 weeks of gestation, the fetus is ready for life outside the uterus. The signal that initiates parturition in humans is still not fully understood, and there seems to be a difference between primates and other mammals. In primates, the primary signal is thought to arise from the fetoplacental unit (i.e. the fetus plus the placenta) as an increase in dehydroepiandrosterone (DHEA) production from the fetal adrenal cortex (Chapter 49), which may be driven by placental (rather than hypothalamic) production of corticotrophin-releasing hormone (CRH) (Chapters 44 and 49; Fig. 52a). DHEA is a precursor for oestrogen production by the placenta. As the placental aromatase enzymes are not rate limiting, an increase in DHEA, which is a precursor of oestrogen (Chapter 50), automatically increases oestrogen production. Whatever the initiating signal might be, the end result is an increase in the synthesis of prostaglandins E and F by fetal and uterine tissues, with concomitant increases in prostaglandin receptors in the uterine smooth muscle. The prostaglandins stimulate the production of uterine receptors for oxytocin and change the pattern of activity in the uterine myometrium from slow, gentle contractions to regular, deep contractions that eventually move the fetus into the cervix. The cervix, which is softened by prior release of the prostaglandins, dilates as the fetus is forced downwards. At this time, the amniotic membrane ruptures. Stretching of the cervix activates mechanoreceptors that stimulate a spinal sympathetic reflex which causes myometrial contraction and secretion of oxytocin from the posterior pituitary gland (Chapter 44; Fig. 52a). Oxytocin is a powerful stimulant of uterine smooth muscle that causes further contraction of the myometrium and pushes the fetus further into the cervix, resulting in further stimulation of mechanoreceptors and leading to the release of more oxytocin, i.e. this is a positive feedback system. The spinal reflex, aided by waves of oxytocin, generates large, regular contractions of the uterus that eventually expel the fetus and placenta through the vagina, completing the birth process. Oxytocin continues to be useful, as it limits maternal bleeding by causing vasoconstriction. In the fetus, oxytocin closes the ductus arteriosus, a blood vessel that shunts blood away from the pulmonary circulation in utero, but which would obviously hamper postpartum life should it remain open.