Alcohol and Alcoholism Vol. 35, No. 6, pp. 554-560, 2000
© 2000 Medical Council on Alcoholism
INFLUENCE OF CHRONIC ALCOHOL INGESTION ON ACETALDEHYDE-INDUCED DEPRESSION OF RAT CARDIAC CONTRACTILE FUNCTION
Department of Pharmacology, Physiology, and Therapeutics, University of North Dakota School of Medicine, 501 N. Columbia Road, Grand Forks, ND 58203 and
1 Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201, USA
Received 27 March 2000; first review notified 23 May 2000; accepted 29 May 2000
Long-standing ethanol consumption acts as a chronic cardiac stress and often leads to alcoholic cardiomyopathy. We have recently shown that the acute ethanol-induced depression in myocardial contraction was substantiated by chronic 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 ventricular papillary muscles and myocytes from rats fed with control or ethanol-enriched diet. Muscles and myocytes were electrically stimulated at 0.5 Hz and contractile properties analysed included peak tension development (PTD) and peak shortening (PS). Intracellular Ca2+ transients were measured as fura-2 fluorescence intensity changes (
FFI). Papillary muscles from ethanol-consuming animals exhibited reduced baseline PTD and attenuated responsiveness to increase of extracellular Ca2+. Acute ACA (0.3–10 mM) addition elicited a dose-dependent depression of PTD. However, the inhibition magnitude was significantly reduced in ethanol-treated rats. Myocytes from both control and ethanol-treated rats exhibited comparable ACA-induced depression in both PS and FFI. Collectively, these data suggest that the ACA-induced depression of myocardial contraction is reduced at the multicellular level, but unchanged at the single cell level, following chronic ethanol ingestion.
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