PREECLAMPSIA - AN ENDOTHELIAL-CELL DISORDER
PREECLAMPSIA - AN ENDOTHELIAL-CELL DISORDER
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DOI：
10.1016/0002-9378(89)90665-0
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发表时间：
1989-11-01
影响因子：
9.8
通讯作者：
MCLAUGHLIN, MK
中科院分区：
文献类型：
--
作者：
ROBERTS, JM;TAYLOR, RN;MCLAUGHLIN, MK
尽管有大量的研究，先兆子痫仍然是一个谜，是孕产妇和胎儿发病率和死亡率的主要原因。大多数研究工作都集中在这种疾病的高血压部分，而对其他同样重要的特征的关注较少。对升压剂的敏感性增加和凝血级联反应的激活发生在先兆子痫的早期，通常先于临床可识别的疾病。由于内皮细胞损伤减少血管舒张剂的合成，增加血管收缩剂的产生，损害内源性抗凝剂的合成，并增加促凝血剂的产生，这些细胞可能与先兆子痫的病理生理学有关。事实上，内皮细胞损伤的证据是由先兆子痫最典型的形态学病变--肾小球内皮增生提供的。对这一假设的额外支持来自于表明先兆子痫妇女血液中存在的循环纤连蛋白（其可以从受损的内皮细胞释放）水平增加和因子VIII抗原增加的报告。最近，直接的证据表明，在体外损伤内皮细胞和增加收缩敏感性的孤立的血管的活动已经提出。我们认为，灌注不良的胎盘组织释放一种因子进入体循环，损伤内皮细胞。由内皮细胞损伤引起的变化引起了凝血、血管收缩和血管内液体再分布的功能障碍级联反应，导致先兆子痫的临床综合征。
Despite intense study preeclampsia remains enigmatic and a major cause of maternal and fetal morbidity and mortality. Most investigative efforts have focused on the hypertensive component of this disorder with reduced attention given to other equally important characteristics. Increased sensitivity to pressor agents and activation of the coagulation cascade occur early in the course of preeclampsia, often antedating clinically recognizable disease. Inasmuch as endothelial cell injury reduces the synthesis of vasorelaxing agents, increases the production of vasoconstrictors, impairs synthesis of endogenous anticoagulants, and increases procoagulant production, these cells are likely to be implicated in the pathophysiology of preeclampsia. Indeed, evidence of endothelial cell injury is provided by the most characteristic morphologic lesion of preeclampsia, glomerular endotheliosis. Additional support for this hypothesis is derived from reports that indicate increased levels of circulating fibronectin (which can be released from injured endothelial cells) and increased factor VIII antigen present in the blood of preeclamptic women. More recently, direct evidence of activities that injure endothelial cells in vitro and increase the contractile sensitivity of isolated vessels has been presented. We propose that poorly perfused placental tissue releases a factor(s) into the systemic circulation that injures endothelial cells. The changes initiated by endothelial cell injury set in notion a dysfunctional cascade of coagulation, vasocostriction, and intravascular fluid redistribution that results in the clinical syndrome of preeclampsia.