Robertson W B, Brosens I, Dixon G
Perspect Nephrol Hypertens. 1976;5:115-27.
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.
为建立血绒毛膜胎盘形成，无绒毛滋养层穿透基蜕膜中的螺旋动脉，随后沿动脉向下迁移至子宫肌层中的母本放射状动脉。血管内滋养层与母体血管壁组织之间的相互作用（生理变化）使这些动脉适应子宫胎盘动脉，这些大口径血管排空至绒毛间隙。反应性肌弹性血管组织的丧失导致外周阻力降低，从而使进入绒毛间隙的血流量大幅增加。在子痫前期妊娠中，孕中期继发性血管内滋养层迁移受到抑制，因此子宫胎盘动脉的子宫肌层段仍为反应性肌弹性动脉。随着临床子痫前期的发作，急性动脉粥样硬化，一种坏死性动脉病，影响胎盘床的小肌性动脉和真蜕膜中的小动脉。当原发性高血压并发子痫前期时，胎盘床动脉表现为增生性动脉硬化和急性动脉粥样硬化的组合。有证据表明，血绒毛膜胎盘形成的建立需要胎儿和母体组织之间受控的免疫反应，并且不适当的免疫反应可能参与子痫前期动脉病的发病机制。
