Fetal Alcohol Syndrome (FAS) consists of a constellation of pathologies and functional/development abnormalities resulting from alcohol exposure in the womb. Medical problems related to FAS include retarded body and mental development, craniofacial abnormalties and cardiac structural and functional deficits. Some of these abnormalities appear due to alcohol-induced death of neural crest cells which migrate fromthe developing nervous system and give rise to structual and functional components of many organ systems, including the autonomic nervous system. It is hypothesized that underpopulation of the cardiac parasympathetic intrinsic nervous system may result from cell death and insufficient neural crest cell migration. This could explain the tachycardia and other functional cardiac pacing abnormalities observed in FAS infants. The population densities of cardiac intrinsic parasympathetic ganglion cells in ethanol- exposed and control rats will be assessed pre- and post-natally by histochemical and immunohistochemical techniques. It is also hypothesized that alcohol-induced redution in protein sysnthesis may inhibit the synthesis of Atrial Natriuretic peptide (ANP) in fetal atria and ventricles. ANP is a cardiovascular hormone with potent antihypertensive and vasoregulatory properties as well as antimitotic functions. Therefore, alteration in ANP content may affect cardiac development. Cardiac ANP content willb e monitored pre- and post- natally in ethanol-exposed and control rats by immunohistochemistry and radioimmunoassay. The results of the proposed studies should contribute significantly to understanding of the etiology of cardiac functional deficits related to FAS and lead to future studies at the molecular and cell biological levels of cardiac structural and functional abnormalities.
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