Cocaine does not affect prostacyclin, thromboxane or prostaglandin E production in human umbilical veins

Abstract

Vasoactive prostaglandins have been reported to mediate umbilical/placental blood flow in humans. Since it has been suggested that cocaine exerts its teratogenic action via vasoconstriction and a corresponding reduction in blood flow, it is reasonable to hypothesize that cocaine influences the vasoactive prostaglandins such that blood flow would be affected. The purpose of this study, therefore, was to determine the effects of cocaine on the vasoactive prostaglandins prostacyclin, thromboxane, and prostaglandin E, using human umbilical veins. Prostacyclin (PGI 2), thromboxane (TXA 2), and prostaglandin E (PGE) levels were measured from human umbilical veins collected at term. The veins were perfused in a closed system with either a 50 μg/ml, a 100 μg/ml, a 200 μg/ml, or a 400 μg/ml cocaine solution for 60 min, and the prostaglandins were measured by radioimmunoassay of their stable metabolites. Data were analyzed by ANOVA, and post-hoc analyses were performed by Fisher's Protected Least Significant Difference Test. Cocaine did not influence PGI 2, TXA 2, or PGE production ( Ps > 0.05) in this series of studies. Thus, contraction of human umbilical vessels and decreased blood flow in human umbilical vessels does not appear to be mediated by changes in the vasoactive prostaglandins.