Uterine Blood Flow

Blood flow to the uterus increases from about 50 to 100 mL/min in the midluteal phase of the menstrual cycle to more than 1 L/min in the third trimester. At term, uterine blood flow, of which more than 80% is directed to the placental implantation site, accounts for about 15 to 20% of the cardiac output. Increased flow begins shortly after implantation, before formation of the placenta is complete, and rises progressively in parallel with expansion of the uterine mass. Decreased resistance of the small myometrial arteries that lie under and around the implantation site is evident as early as the fifth week and well before similar changes are seen in larger arteries. These early changes are thought to reflect invasion of the spiral arteries by the syncytiotrophoblast and their consequent dilatation. In animal studies, the absence of autoregulation, as indicated by the lack of reactive hyperemia following a brief arterial occlusion, suggests that arterioles in the gravid uterus may be maximally dilated under basal conditions. The decrease in resistance is so pronounced that some investigators refer to the uteroplacental circulation as an arterio-venous shunt.

It may be recalled from the discussion in Chapter 47 that concentrations of estrogens and progesterone in maternal blood plasma increase steadily and dramatically as pregnancy progresses. Evidence from both animal and human studies indicates that estrogens have vasodilatory effects and decrease vascular resistance, especially in the uterus, which is particularly sensitive to this hormonal effect. Estrogens also markedly lower sensitivity of the uterine vasculature to vasoconstrictor agents. Extensive studies of uterine blood flow have been made in pregnant sheep, which have been studied as models for human pregnancy. Infusions of physiologically relevant amounts of angiotensin II or norepineph-rine produce little effect on uterine vascular smooth muscle or uteroplacental blood flow, although at the same concentrations these agents cause significant constriction of extrauterine vasculature and increased systemic blood pressure. In fact, infusion of angio-tensin II into pregnant ewes actually increases uterine blood flow as a consequence of increased systemic blood pressure. Precisely how the uterine vasculature becomes desensitized to pressor agents has not been established, but some evidence suggests that ovarian and placental hormones stimulate local production of vasodilator agents, including nitric oxide and prostacyclin (PGI2).

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