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Acute effects of ethanol on action potential and intracellular Ca(2+) transient in cardiac ventricular cells: a simulation study
M. Pásek, M. Bébarová, G. Christé, M. Šimurdová, J. Šimurda,
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't
Grant support
NT14301
MZ0
CEP Register
NLK
ProQuest Central
from 1997-01-01 to 1 year ago
Medline Complete (EBSCOhost)
from 2003-01-01 to 1 year ago
Nursing & Allied Health Database (ProQuest)
from 1997-01-01 to 1 year ago
Health & Medicine (ProQuest)
from 1997-01-01 to 1 year ago
- MeSH
- Action Potentials drug effects MeSH
- Models, Biological MeSH
- Ethanol pharmacology MeSH
- Intracellular Space drug effects metabolism MeSH
- Myocytes, Cardiac drug effects metabolism MeSH
- Rats MeSH
- Humans MeSH
- Computer Simulation * MeSH
- Sarcoplasmic Reticulum drug effects metabolism MeSH
- Heart Ventricles cytology MeSH
- Calcium metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Alcohol consumption may result in electrocardiographic changes and arrhythmias, at least partly due to effects of ethanol on cardiac ionic currents. Contractility and intracellular Ca(2+) 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 Ca(2+) 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 ≥8 mM). These changes were almost exclusively caused by the ethanol-induced alterations of I K1. The cytosolic Ca(2+) 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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