ENDOGENOUS NITRIC-OXIDE ATTENUATES ETHANOL-INDUCED VASOCONSTRICTION IN THE HUMAN PLACENTA

The purpose of this study was to clarify the role of endogenous nitric oxide and prostanoids in ethanol-induced perturbation of microcircula tion in perfused human placenta. Infusion of ethanol into chorionic pl ate vessels at 10-65 mM increases perfusion pressure in a concentratio n-dependent fashion, and is an indicator of fetal-placental vasoconstr iction. Simultaneous infusion of N-omega-nitro-L-arginine, methylene b lue and endothelial cell removal significantly enhances the ethanol-in duced increase in perfusion pressure. In contrast, sodium nitroprussid e attenuates this effect. Indomethacin did not significantly modify th e ethanol-induced response. In conclusion, inhibition of the action of endogenous nitric oxide is associated with an increase in fetal-place ntal vasoconstriction. These results suggest that endogenous nitric ox ide acts as a vasodilator that reduces ethanol-induced vasoconstrictio n, thus improving microcirculation, and leads to decreased placental d amage.