PRESSER EFFECT OF ETHANOL IN THE ISOLATED-PERFUSED HUMAN PLACENTAL LOBULE

Pharmacologically relevant concentrations of ethanol (0.01-0.3 g/%) we re perfused via the fetal circulation in isolated human placental lobu les. This resulted in a dose-related rise in fetal arterial pressure, which at 0.3 g/% ethanol, was 10.1+/-1.1 mmHg above the pre-drug basel ine. The presser responses to ethanol were (i) rapid in onset, reachin g a stable plateau within 5-10 min following administration, (ii) read ily reversible by perfusion with drug-free media, (iii) non-tachyphyla ctic and (iv) largely inhibited by the cyclo-oxygenase inhibitor, indo methacin (5 mu M). This presser action of ethanol in the fetal circula tion may contribute to the pathogenesis of the fetal alcohol syndrome as well as represent an underlying mechanism of ethanol-induced hypert ension.