Alcohol and fetoplacental vasoconstrictor reactivity.

摘要

Alcohol abuse during pregnancy is a well-known factor in fetalmorbidity, including smaller fetal size. We have shown thatchronic hypoxia, considered the main pathogenetic factor inintrauterine growth restriction, elevates fetoplacental vascularresistance (and vasoconstrictor reactivity) and thus, presumably,reduces placental blood flow. We thus hypothesized that alcoholmay affect the fetus – in addition to other mechanisms – byaltering fetoplacental vascular resistance and/or reactivity. Usingisolated, double-perfused rat placenta model, we found thatmaternal alcohol intake in the last third of gestation doubled thevasoconstrictor responses to angiotensin II but did not affectresting vascular resistance. Reactivity to acute hypoxic challengeswas unchanged. Chronic maternal alcohol intake in a rat modelalters fetoplacental vasculature reactivity; nevertheless, thesechanges do not appear as serious as other detrimental effects ofalcohol on the fetus.