Urinary prostacyclin and thromboxane metabolites in drinking pregnant women and in their infants: relations to the fetal alcohol effects.

To study the effect of maternal ethanol consumption on the production of prostacyclin and thromboxane, we measured urinary 6-keto-prostaglandin F1 alpha (a hydration product of prostacyclin), 2,3-dinor-6-keto-prostaglandin F1 alpha (generated from 6-keto-prostaglandin F1 alpha through beta oxidation), and thromboxane B2 (a hydration product of thromboxane A2) using consequent high-performance liquid chromatography and radioimmunoassays in 39 drinking women and 16 abstinent controls, and in their infants. Thirty-one drinkers and two control women smoked. Maternal ethanol consumption was accompanied by increased output of prostacyclin and thromboxane metabolites in the mothers, but no relationship was apparent between the increased metabolites and development of fetal alcohol effects in 22 mothers. There were no differences between smoking and nonsmoking drinkers in the excretion of these prostanoids. All the infants born to the drinkers had increased thromboxane B2 excretion, but the excretion of prostacyclin metabolites was increased only in infants with fetal alcohol effects. The ratio between prostacyclin and thromboxane was reduced in infants with fetal alcohol effects. Thus, maternal ethanol consumption is associated with enhanced prostacyclin and thromboxane synthesis, perhaps in the kidneys and/or systemic circulation and vascular bed. Similar changes may also occur in the fetus and/or newborn with fetal alcohol effects.