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Am J Physiol Heart Circ Physiol 275: H122-H130, 1998;
0363-6135/98 $5.00
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Vol. 275, Issue 1, H122-H130, July 1998

Chronic alcohol-induced changes in cardiac contractility are not due to changes in the cytosolic Ca2+ transient

Vincent M. Figueredo1,2,3, Kevin C. Chang1,3, Anthony J. Baker1,3, and S. Albert Camacho1,3

1 Department of Medicine (Cardiology) and 2 Ernest Gallo Clinic and Research Center, San Francisco General Hospital, 3 University of California, San Francisco, California 94110

Long-standing heavy alcohol consumption acts as a chronic stress on the heart. It is thought that alcohol-induced changes of contractility are due to altered Ca2+ handling, but no measurements of cytosolic Ca2+ ([Ca2+]c) after chronic alcohol exposure have been made. Therefore experiments were performed to determine whether alcohol-induced changes in contractility are due to altered Ca2+ handling by measuring [Ca2+]c (indo 1) in hearts from rats drinking 36% ethanol for 7 mo and age-matched controls. Peak left ventricular pressure was depressed (-16%), whereas rates of contraction (12%) and relaxation (14-20%) were faster in alcohol-exposed hearts. Systolic [Ca2+]c (808 ± 45 vs. 813 ± 45 nM), diastolic [Ca2+]c (195 ± 11 vs. 193 ± 10 nM), and rates of [Ca2+]c rise and decline were the same in alcohol-exposed and control hearts. Protein levels of Ca2+-handling proteins, sarcoplasmic reticulum Ca2+-ATPase and phospholamban, were the same in myocytes isolated from alcohol-exposed and control hearts (SDS-polyacrylamide gel). These data suggest that chronic alcohol-induced contractile changes are not due to altered Ca2+ handling but may be due to changes at the level of the myofilament. As a first step in elucidating the mechanism(s) of alcohol-induced changes at the myofilament, we assessed myosin heavy chain (MHC) isoform content (SDS-polyacrylamide gel). alpha -MHC was decreased relative to beta -MHC (a/a + b = 0.55 ± 0.03 vs. 0.66 ± 0.02; P < 0.02) in alcohol-exposed hearts, which cannot account for the observed alcohol-induced contractile changes. In conclusion, changes of myocardial contractility due to chronic alcohol exposure do not result from altered Ca2+ handling but from changes at the level of the myofilament that do not involve MHC isoform shifts.

ethanol; myocyte; myosin heavy chain; sarcoplasmic reticulum; adenosinetriphosphatase; phospholamban


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