Alterations in prostaglandin metabolism of cultured human umbilical vein endothelial cells affected by smoking during pregnancy

Abstract

Many endothelial cell functions that exert a regulatory influence on fetal hemodynamics and placental perfusion are modulated by metabolites of arachidonic acid, in particular prostaglandins. We used an in vitro model system to study the possible role of the vascular endothelium in the pathogenesis of chronic placental insufficiency. We examined cell growth behavior and prostaglandin metabolism in cultured umbilical vein endothelial cells from mothers exposed to the risk factor smoking during pregnancy (n=18) and compared them with healthy non-smoking control mothers (n=20). Endothelial cells from smoking mothers grew less readily than control cells. The synthesis of the prostaglandins PGI 2 and PGE 2 , both potent vasodilators and platelet aggregation inhibitors, was reduced significantly in endothelial cells from smoking mothers. Thus, if this change also occurs in the placenta, reduced prostaglandin synthesis could contribute to impaired placental perfusion. Our results suggest that prostaglandins may play an important role in the etiology and pathogenesis of chronic placental insufficiency.