Maternal uterine vascular lesions in the hypertensive complications of pregnancy.

Abstract

To establich hemochorial placentation, the nonvillous trophoblast breaches the spiral arteries in the basal decidua and later migrates down the arteries as far as the parent radial arteries in the myometrium. Interactions between the endovascular trophoblast and the tissues of the maternal vessel wall (physiological changes) adapt these arteries to the uteroplacental arteries, and these large caliber vessels empty into the intervillous space. Loss of reactive musculoelastic vascular tissue results in a lowering of peripheral resistance, permitting a greatly increased blood flow into the intervillous space. In preeclamptic pregnancies, there is inhibition of the secondary endovascular trophoblast migration in the second trimester, so that the myometrial segments of the uteroplacental arteries remain as responseive musculoelastic arteries. With the onset of clinical preeclampsia, acute atherosis, a necrotizing arteriopathy, affects small muscular arteries in the placental bed and arterioles in the decidua vera. When essential hypertension is complicated by preeclampsia, the placental bed arteries show a combination of hyperplastic arteriosclerosis and acute atherosis. There is evidence that the establishment of hemochorial placentation requires controlled immunological reactions between fetal and maternal tissues and that an inappropriate immune response may be involved in the pathogenesis of the arteriopathy of preeclampsia.