Chronic alcoholism causes a cardiac contractile dysfunction which, in rats, may occur after 6 mo to 1 yr of alcohol consumption. Sepsis, on a more acute basis, can also induce intrinsic cardiac dysfunction. We tested the hypothesis that 2 mo of chronic alcohol feeding, while not directly causing overt depression of the myocardium, might sensitize the heart to a known cardiac stress, i.e., sepsis. We proposed that sepsis, induced in an alcoholic animal, would cause a more severe myocardial depression than in a nonalcoholic rat. Thus rats were fed a liquid diet with 36% of the total calories as alcohol for 8-10 wk and were then anesthetized and received an injection of live Escherichia coli (approximately 10(10) E. coli) through a dorsal subcutaneous catheter followed by a second dose approximately 5 h later. The following day, hearts were removed and, using the isolated working heart preparation, intrinsic contractile performance was assessed by generating ventricular function curves. Four groups of animals were studied. Hearts from the nonalcoholic-nonseptic group and the alcoholic-nonseptic group showed identical cardiac work (cardiac output x peak systolic pressure at the highest preload was 6,113 +/- 324 and 5,955 +/- 406 ml.min-1.mmHg-1, respectively). Work in the nonalcoholic-septic and the alcoholic-septic groups was decreased by 30 and 50%, respectively (4,806 +/- 478 vs. 2,917 +/- 435 ml.min-1.mmHg-1 at the highest preload). Thus 2 mo chronic alcohol consumption caused no overt cardiac dysfunction by itself but did exacerbate the myocardial injury induced by sepsis.