In our recent work, we studied the effects of ethanol on electrical activity of rat ventricular myocytes (1, 2). The results showed that ethanol can effectively affect the action potential (AP) and the principal membrane ionic currents, namely the fast sodium current (INa), L-type calcium current (ICa), transient outward potassium current (Ito) and inward rectifier potassium current (IK1). The effect on INa, ICa and Ito was inhibitory while the effect on IK1 was dual; ethanol caused an inhibition of IK1 at concentrations up to 0.8 mM and its activation at concentrations above 20 mM. The effect of ethanol on rat AP included a decrease of maximum upstroke velocity, AP amplitude and AP duration (APD). In this work, the concentration dependences of ethanol-induced inhibition/activation of ionic currents derived from experimental data (1, 2) were incorporated into the published model of rat ventricular cardiomyocyte (3) with the aim to assess the share of ionic current components in ethanol-induced changes of AP configuration. The model reproduced well the reduction of APD under the effect of ethanol. APD90 (at 90% repolarization) was decreased by 9.7% at 50 mM ethanol which compared with our experimental data (7.2 ± 2.2 %, n = 5). This change was almost exclusively caused by an increase of IK1, a current that exhibited the highest sensitivity to ethanol in our experiments. Further increase of ethanol concentration to 340 mM caused a reduction of APD mainly at 50% repolarization (APD50) which resulted from the increased inhibition of ICa.In the following step, we tentatively incorporated the known concentration dependences of ethanol-induced changes of ionic current components evaluated from available experimental results (1, 2, 4) into a model of human ventricular cardiomyocyte (5) to obtain at least a rough estimate of ethanol effect in human cardiac cells. Changes of AP in this model were explored at ethanol concentration 21.8 mM (1‰), 43.6 mM (2‰) and 65.3 mM (3‰) that correspond to mild, middle and heavy alcohol intoxication. Unlike the effect in rat cardiomyocytes, the increase of ethanol concentration in the human model resulted in the prolongation of both APD50 (by 1.9%, 4.5% and 6.8%, respectively) and APD90 (by 0.2%, 2.8% and 5.1%, respectively) due to the inhibition of IKr (4). Our results suggest that contribution of individual ionic current components to the effect of ethanol on AP repolarization in cardiac cell is strongly dependent on species differences in current densities. Because AP configuration in the human model shows only a small sensitivity to variations of IK1, the effect of ethanol-induced inhibition of IKr predominates implying prolongation of APD. This effect might contribute to the clinically observed prolongation of QT interval under consumption of alcohol.