![]() ![]() ![]() To do this, we will focus on ethanol's effects upon in utero cardiomyocyte development and ventricular formation with a potential impact upon structure-function relationships. For this postulate to be critically tested, we must establish the rat FAE model. Because cardiomyocyte proliferation occurs almost exclusively during embryonic and fetal heart development, we postulate that FAE will reduce the total myocyte cell number in the ventricle. Based on these data, AND information available from the literature, we hypothesize that in utero FAE will modify heart development by mechanisms that remain to be fully elucidated. Our preliminary data suggest that several biochemical and molecular indices of heart development are altered in ventricles from FAE male and female offspring. Nevertheless, a rat, fetal alcohol exposure (FAE) model that recapitulates some of the FAS CV-defects found in man has not been firmly established. ![]() The cardiovascular (CV) system is a common site of spontaneous as well as pharmacologically-induced birth defects that are associated with high morbidity and mortality. ![]()
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