Effect of ethanol on thromboxane and prostacyclin production in the human placenta

Fetal alcohol syndrome (FAS) is frequently associated with intrauterine gro wth retardation (IUGR). One cause of ethanol-induced IUGR is thought to be related to increased presser activity in the human placenta, resulting in d ecreased oxygenation and nutrient transport to the fetus. Thus, we have inv estigated the effect of ethanol on paracrine substances, such as thromboxan e and prostacyclin, that act as vasoregulators within the intrauterine tiss ues. In these studies we have utilized the perfused single human cotyledon system to study the effect of ethanol on placental prostanoid production. W e assessed the effect of longer (240 min) and more acute (60 min) exposure to ethanol on release of thromboxane B-2 (TxB(2)) and 6-keto-prostaglandin F-1 alpha (6-keto-PGF(1 alpha)) at the maternal and fetal sides of the plac enta. Thromboxane was increased by both longer and shorter ethanol exposure , especially on the fetal side of the placenta. Prostacyclin was essentiall y unchanged with exposure to ethanol. The thromboxane:prostacyclin ratio al so tended to increase with both 60- and 240-min ethanol exposure, but a sta tistically significant increase was seen only at a few time points. In the 60-min ethanol exposure, an increase in thromboxane was observed both durin g and following exposure to ethanol. The increase in the thromboxane milieu observed with ethanol exposure may lead, at least in part, to the IUGR whi ch is frequently associated with FAS. Prevention of this effect of ethanol on thromboxane production might be a beneficial intervention for FAS. (C) 2 000 Elsevier Science Inc. All rights reserved.