Open AccessAlcohol and Fetoplacental Vasoconstrictor Reactivity
Author(s) -
Vít Jakoubek,
Václav Hampl
Publication year - 2018
Publication title -
physiological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 70
eISSN - 1802-9973
pISSN - 0862-8408
DOI - 10.33549/physiolres.933609
Subject(s) - fetus , placenta , endocrinology , medicine , gestation , hypoxia (environmental) , angiotensin ii , alcohol , vascular resistance , intrauterine growth restriction , pregnancy , reactivity (psychology) , renin–angiotensin system , biology , chemistry , hemodynamics , oxygen , receptor , blood pressure , pathology , biochemistry , genetics , organic chemistry , alternative medicine
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.