Acute effects of ethanol on action potential and intracellular Ca2+ transient in cardiac ventricular cells: a simulation study



Year of publication 2016
Type Article in Periodical
Magazine / Source Medical & Biological Engineering & Computing
MU Faculty or unit

Faculty of Medicine

Field Physiology
Keywords Ethanol; Cardiomyocyte; Action potential; Rat ventricular cell model; Human ventricular cell model
Description Alcohol consumption may result in electrocardiographic changes and arrhythmias, at least partly due to effects of ethanol on cardiac ionic currents. Contractility and intracellular Ca2+ dynamics seem to be altered as well. In this study, we integrated the available (mostly animal) experimental data into previously published models of the rat and human ventricular myocytes to assess the share of ionic current components in ethanol-induced changes in AP configuration and cytosolic Ca2+ transient in ventricular cardiomyocytes. The rat model reproduced well the experimentally observed changes in AP duration (APD) under ethanol (slight prolongation at 0.8 mM and shortening at a parts per thousand yen8 mM). These changes were almost exclusively caused by the ethanol-induced alterations of I (K1). The cytosolic Ca2+ transient decreased gradually with the increasing ethanol concentration as a result of the ethanol-induced inhibition of I (Ca). In the human model, ethanol produced a dose-dependent APD lengthening, dominated by ethanol effect on I (Kr), the key repolarising current in human ventricles. This effect might contribute to the clinically observed proarrhythmic effects of ethanol in predisposed individuals.
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