Pressor effect of ethanol in the isolated perfused human placental lobule

Pharmacologically relevant concentrations of ethanol (0.01-0.3 g/%) were perfused via the fetal circulation in isolated human placental lobules. 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 baseline. The pressor responses to ethanol were (i) rapid in onset, reaching a stable plateau within 5-10 min following administration, (ii) readily reversible by perfusion with drug-free media, (iii) non-tachyphylactic and (iv) largely inhibited by the cyclo-oxygenase inhibitor, inhibitor, indomethacin (5 microM). This pressor action of ethanol in the fetal circulation may contribute to the pathogenesis of the fetal alcohol syndrome as well as represent an underlying mechanism of ethanol-induced hypertension.