Increase in vasoactive prostaglandin E production after perfusion in human placental cotyledons.

Studies from our laboratory indicate that prostaglandins may be mediators of at least some of the teratogenic actions of ethanol in both mouse and human tissue model systems. The present studies were designed to evaluate the relationship between ethanol and prostaglandin E (PGE) production in isolated human placental cotyledons. Placentas were obtained immediately after cesarean section delivery. A fetal artery supplying a single cotyledon was identified and cannulated, and the isolated cotyledon was placed in a perfusion chamber where maternal circulation was established and dual circulation continued throughout the perfusion procedure. Antipyrine clearance, oxygen consumption, and placental production of human chorionic gonadotropin were measured to verify tissue viability. PGE levels of the perfusate were measured by radioimmunoassay. Study 1 evaluates the effect of perfusion with 25 and 100 mM ethanol on placental PGE production. It was found that PGE production increased after perfusion with 25 mM ethanol, but not during the perfusion period per se. The paradigm for study 2 was identical to that of study 1, with the addition of a buffer washout period after 100-mM ethanol perfusion. Again, results indicate that perfusate PGE levels were increased in the buffer washout periods after the 25-mM and the 100-mM ethanol perfusions. The effect was not concentration dependent. An increase in circulating PGE associated with ethanol administration may be teratogenic actions and represent a potential mechanism underlying at least some aspects of fetal alcohol syndrome.