Preeclampsia: an endothelial cell disorder.

摘要: Despite intense study preeclampsia remains enigmatic and a major cause of maternal fetal morbidity mortality. Most investigative efforts have focused on the hypertensive component this disorder with reduced attention given to other equally important characteristics. Increased sensitivity pressor agents activation coagulation cascade occur early in course preeclampsia, often antedating clinically recognizable disease. Inasmuch as endothelial cell injury reduces synthesis vasorelaxing agents, increases production vasoconstrictors, impairs endogenous anticoagulants, procoagulant production, these cells are likely be implicated pathophysiology preeclampsia. Indeed, evidence is provided by most characteristic morphologic lesion glomerular endotheliosis. Additional support for hypothesis derived from reports that indicate increased levels circulating fibronectin (which can released injured cells) factor VIII antigen present blood preeclamptic women. More recently, direct activities injure vitro increase contractile isolated vessels has been presented. We propose poorly perfused placental tissue releases factor(s) into systemic circulation injures cells. The changes initiated set motion dysfunctional coagulation, vasoconstriction, intravascular fluid redistribution results clinical syndrome