Prenatal exposure to alcohol: mechanisms of cerebral vascular damage and lifelong consequences

Alcohol is a well-known teratogen, and prenatal alcohol exposure (PAE) leads to a greater incidence of many cardiovascular-related pathologies. Alcohol negatively impacts vasculogenesis and angiogenesis in the developing fetal brain, resulting in fetal alcohol spectrum disorders (FASD). Ample precli...

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Bibliographic Details
Published inAdvances in Drug and Alcohol Research Vol. 2; p. 10818
Main Authors Saha, Partha S, Mayhan, William G
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 21.11.2022
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Summary:Alcohol is a well-known teratogen, and prenatal alcohol exposure (PAE) leads to a greater incidence of many cardiovascular-related pathologies. Alcohol negatively impacts vasculogenesis and angiogenesis in the developing fetal brain, resulting in fetal alcohol spectrum disorders (FASD). Ample preclinical evidence indicates that the normal reactivity of cerebral resistance arterioles, which regulate blood flow distribution in response to metabolic demand (neurovascular coupling), is impaired by PAE. This impairment of dilation of cerebral arteries may carry implications for the susceptibility of the brain to cerebral ischemic damage well into adulthood. The focus of this review is to consolidate findings from studies examining the influence of PAE on vascular development, give insights into relevant pathological mechanisms at the vascular level, evaluate the risks of ethanol-driven alterations of cerebrovascular reactivity, and revisit different preventive interventions that may have promise in reversing vascular changes in preclinical FASD models.
Bibliography:Reviewed by: Anna Bukiya, University of Tennessee Health Science Center (UTHSC), United States
Edited by: Declan Ali, University of Alberta, Canada
Amy Gardiner, University of New Mexico, United States
ISSN:2674-0001
2674-0001
DOI:10.3389/adar.2022.10818