Cg. Acevedo et al., ENDOGENOUS NITRIC-OXIDE ATTENUATES ETHANOL-INDUCED VASOCONSTRICTION IN THE HUMAN PLACENTA, Gynecologic and obstetric investigation, 44(3), 1997, pp. 153-156
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.