The metabolic, functional and electrical effects of ethanol were studied in the isolated isovolumic rat heart retrogradely perfused at constant flow using phosphorus-31 nuclear magnetic resonance spectroscopy and surface electrogram recordings. Ethanol (0.75 to 6.0 vol%; 128 to 1024 mm) caused a concentration-dependent decline in developed pressure without a change in adenosine triphosphate, phosphocreatine, inorganic phosphate or pH. Ethanol (6%) caused abolition of electrical activity. The functional decline could be rapidly and completely reversed by perfusing with ethanol-free solution and, significantly although not completely, reversed by increasing perfusate calcium to 4 mm. Furthermore, ethanol shifted the perfusate calcium-tetanic pressure relationship in the presence of ryanodine (1 μm) downwards and to the right. The results suggest ethanol's acute effects in this model are not mediated by changes in energy metabolism or cellular pH, but rather by sarcolemmal effects and by a decrease in both myofilament calcium sensitivity and maximal force generating ability.
- Excitation-contraction coupling
- High energy phosphates
- Left ventricular function
ASJC Scopus subject areas
- Molecular Biology
- Cardiology and Cardiovascular Medicine