[Functional differentiation of the vascular endothelium in high risk pregnancies]

Endothelial cell functions regulating fetal hemodynamics and placental perfusion are modulated by metabolites of arachidonic acid, in particular derivatives of cyclooxygenase such as prostaglandins. We utilized an in vitro system to study the possible role of the vascular endothelium in the pathogenesis of chronic placental insufficiency. Cellular growth and prostaglandin metabolism were investigated in cultured umbilical vein endothelial cells from mothers exposed to risk factors such as smoking and diabetes mellitus during pregnancy. The study comprised cells from smoking (n = 18) and diabetic mothers (n = 5) compared to non-smoking, non-diabetic controls (n = 20). Endothelial cells from smoking and diabetic mothers grew less readily than did control cells. The synthesis of the prostaglandins PGI2 and PGE2, both potent vasodilators and platelet aggregation inhibitors, was significantly reduced in endothelial cells from smoking mothers and from mothers suffering from diabetes of various stages. Thus, reduced prostaglandin synthesis may be a cause of impaired placental perfusion in high risk pregnancies. Our data suggest that prostaglandins may play an important role in the etiology and pathogenesis of chronic placental insufficiency.