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• W2974679145 abstract "Alcohol abuse during pregnancy is a well-known factor in fetal morbidity, including smaller fetal size. We have shown that chronic hypoxia, considered the main pathogenetic factor in intrauterine growth restriction, elevates fetoplacental vascular resistance (and vasoconstrictor reactivity) and thus, presumably, reduces placental blood flow. We thus hypothesized that alcohol may affect the fetus – in addition to other mechanisms – by altering fetoplacental vascular resistance and/or reactivity. Using isolated, double-perfused rat placenta model, we found that maternal alcohol intake in the last third of gestation doubled the vasoconstrictor responses to angiotensin II but did not affect resting vascular resistance. Reactivity to acute hypoxic challenges was unchanged. Chronic maternal alcohol intake in a rat model alters fetoplacental vasculature reactivity; nevertheless, these changes do not appear as serious as other detrimental effects of alcohol on the fetus." @default.
• W2974679145 created "2019-09-26" @default.
• W2974679145 creator A5016527328 @default.
• W2974679145 creator A5083856804 @default.
• W2974679145 date "2018-06-23" @default.
• W2974679145 modified "2023-09-27" @default.
• W2974679145 title "Alcohol and Fetoplacental Vasoconstrictor Reactivity" @default.
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• W2974679145 doi "https://doi.org/10.33549/physiolres.933609" @default.
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