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机构地区:[1]第一军医大学南方医院妇产科,广州510515
出 处:《广东医学》2002年第7期685-686,共2页Guangdong Medical Journal
基 金:广东省社会重大问题联合攻关项目基金资助 (编号 :2KM0 560 1S)
摘 要:目的 通过对妊高征合并胎儿宫内发育迟缓胎盘的光镜和电镜观察 ,了解妊高征合并IUGR的胎盘病理改变 ,从而探讨妊高征引起IUGR的原因。方法 选取妊高征合并IUGR患者及正常妊娠妇女胎盘各 3 0例 ,常规HE染色及PAS染色 ,观察胎盘形态学变化。另取妊高征合并IUGR及正常胎盘各 5例 ,5 0 0H型透射电镜观察。结果 观察组绒毛间质纤维化及纤维素样坏死 >3 %、绒毛间质白细胞浸润、合体滋养细胞结节 >3 0 %、绒毛血管减少瘀血、细胞滋养细胞增生 >2 0 %、滋养细胞基底膜增厚 >3 %的数量均明显高于对照组 ,电镜发现合体滋养细胞超微结构改变明显 ,蜕膜螺旋动脉内皮损伤 ,管腔狭窄 ,部分动脉末端闭塞。结论 妊高征引起IUGR的病理改变主要有三方面 :绒毛毛细血管减少、瘀血 ;血管合体膜增厚 ;蜕膜螺旋动脉狭窄、闭塞。这也是妊高征造成IUGR的病理学原因。Objective To study the pathological change of placenta in pregnancy-induced hypertension(PIH) complicated with intrauterine growth retardation by microscope and electron microscope and to discuss the pathogenesis of intrauterine growth retardation associated PIH. Methods Placental samples were collected from 30 pregnancies with PIH complicated with IUGR and from 30 normal pregnant women. The tissue sections were assessed for morphological change with HE-and PAS-stain section. 5 samples from each group were also examined by electron microscope. Results The numbers of stroma fibrosis and fibrinoid necrosis of villi >3%, stroma leucocyte soakage of villi and villous syncytial knots>30%, decreased and congestion villous vascular, and prdiferating cytotrophoblasts>20% and thicking of basal lamina>3% were significantly higher in the group with placenta of PIH complicated with IUGR than that of normal group. Ultrastructural changes of syncytiotrophoblast, decidua spiral artery endodermis damnification, artery cavity straitness and partialarterial extremity obstruction were obsersed by electron microscope. Conclusion The pathological changes of IUGR induced by PIH are decreased villous capillary vessel and congestion, vasculosyncytial membranes incrassation, decidua spiral artery straitness and obstruction, which are the pathological cause of IUGR in PIH.
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