Soma H, Yoshida K, Mukaida T, Tabuchi Y
Contrib Gynecol Obstet. 1982;9:58-75.
Pregnancy complicated by hypertension is commonly associated with placental insufficiency, thereby resulting in fetal growth retardation. Furthermore, reduced utero-placental blood flow has been recognized in cases of severe preeclampsia with hypertension. Thus, it must be assumed that histological as well as ultrastructural findings in hypertensive placentas are due to the occlusion or narrowing of the uteroplacental vasculature as well as placental ischemia. Microscopically, these placental changes include infarcts, increased syncytial knots, hypovascularity of the villi, cytotrophoblastic proliferation, thickening of the trophoblastic basement membrane, obliterative enlarged endothelial cells in the fetal capillaries and atherosis of the spiral arteries in the placental bed. In addition, ultrastructural features are characterized by a decreased number of syncytial microvilli, proliferation of cytotrophoblastic cells, focal syncytial necrosis, thickening of trophoblastic basement membrane and narrowing of the fetal capillaries, as a number of studies have demonstrated. These placental abnormalities can be seen not only in human toxemia, but also in animals with experimentally induced toxemia or with spontaneous toxemia.
妊娠期并发高血压通常与胎盘功能不全相关,从而导致胎儿生长受限。此外,重度子痫前期伴高血压病例中已发现子宫胎盘血流减少。因此,必须假定高血压胎盘的组织学和超微结构改变是由于子宫胎盘血管闭塞或狭窄以及胎盘缺血所致。在显微镜下,这些胎盘变化包括梗死、合体结节增多、绒毛血管减少、细胞滋养层细胞增殖、滋养层基底膜增厚、胎儿毛细血管内皮细胞肿大闭塞以及胎盘床螺旋动脉粥样硬化。此外,正如许多研究所表明的,超微结构特征表现为合体微绒毛数量减少、细胞滋养层细胞增殖、局灶性合体细胞坏死、滋养层基底膜增厚以及胎儿毛细血管狭窄。这些胎盘异常不仅可见于人类毒血症,也可见于实验性诱导毒血症或自发性毒血症的动物。