An increase in blood flow on both sides of the placenta throughout gestation is necessary to maintain optimal placental and fetal growth. Inadequate blood flow to the placenta is associated with fetal and placental growth retardation. The normal increase in flow is achieved in both circulations of the placenta by a combination of altered vascular anatomy and changes in both vascular resistance and perfusion pressure. Perfusion pressure itself depends on systemic cardiovascular changes and so changes in the maternal or fetal cardiovascular systems may have profound effects on placental perfusion. This review, however, will deal with the contribution of vascular resistance within the placenta itself to placental blood flow. The hemomonochorial human placenta possesses no vascular response elements within the maternal side of the placenta per se. Rather the vascular response elements which control blood flow to the intervillous space of the placenta lie within the uterine, radial, basal and spiral arteries. As trophoblast invasion of the spiral arteries during the first and early second trimesters of pregnancy removes the musculo-elastic lining of the spiral arteries (Sheppard and Bonnar, 198 l), it is probable that these vessels lose their vascular reactivity. Therefore, blood flow into the intervillous space in normal pregnancy may depend more on vascular reactivity of the uterine, radial or basal arteries or on systemic cardiovascular events and so does not fall within the scope of this review of the control of placental vascular resistance. Ultrasound measurements of blood flow velocity waveforms in umbilical and uterine vessels are being increasingly used in the clinical setting as indices ofvascular impedance and flow to the placenta and, hence, of fetal well-being (Trudinger et al, 1985). In normal pregnancy, there is a progressive increase in umbilical end-diastolic velocity and thus a steady fall in resistance in the fetal-placental circulation (Erskine and Ritchie, 1985). The altered umbilical waveforms seen in pre-eclampsia and/or intrauterine growth retardation, which indicate increased fetal-placental vascular impedance and reduced flow, are associated with increased fetal and neonatal morbidity and mortality. Such observations have led to therapeutic interventions such as low-dose aspirin designed to improve fetal-placental blood flow and hence improve clinical outcome (Trudinger et al, 1988).
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