Influence of chronic alcohol ingestion on acetaldehyde-induced depression of rat cardiac contractile function

Long-standing ethanol consumption acts as a chronic cardiac stress and ofte n leads to alcoholic cardiomyopathy. We have recently shown that the acute ethanol-induced depression in myocardial contraction was substantiated by c hronic ethanol ingestion. Acetaldehyde (ACA), the main ethanol metabolite, has been considered to play a role in ethanol-induced cardiac dysfunction. To evaluate the ACA-induced cardiac contractile response following chronic ethanol ingestion, mechanical properties were examined using left ventricul ar papillary muscles and myocytes from rats fed with control or ethanol-enr iched diet. Muscles and myocytes were electrically stimulated at 0.5 Hz and contractile properties analysed included peak tension development (PTD) an d peak shortening (PS). Intracellular Ca2+ transients were measured as fura -2 fluorescence intensity changes (Delta FFI). Papillary muscles from ethan ol-consuming animals exhibited reduced baseline PTD and attenuated responsi veness to increase of extracellular Ca2+. Acute ACA (0.3-10 mM) addition el icited a dose-dependent depression of PTD. However, the inhibition magnitud e was significantly reduced in ethanol-treated rats. Myocytes from both con trol and ethanol-treated rats exhibited comparable ACA-induced depression i n bath PS and Delta FFI. Collectively, these data suggest that the ACA-indu ced depression of myocardial contraction is reduced at the multicellular le vel, but unchanged at the single cell level, following chronic ethanol inge stion.