Detailed Information on Publication Record
2016
Acute effects of ethanol on action potential and intracellular Ca2+ transient in cardiac ventricular cells: a simulation study
PÁSEK, Michal, Markéta BÉBAROVÁ, Georges CHRISTÉ, Milena ŠIMURDOVÁ, Jiří ŠIMURDA et. al.Basic information
Original name
Acute effects of ethanol on action potential and intracellular Ca2+ transient in cardiac ventricular cells: a simulation study
Authors
PÁSEK, Michal (203 Czech Republic, guarantor, belonging to the institution), Markéta BÉBAROVÁ (203 Czech Republic, belonging to the institution), Georges CHRISTÉ (250 France), Milena ŠIMURDOVÁ (203 Czech Republic, belonging to the institution) and Jiří ŠIMURDA (203 Czech Republic, belonging to the institution)
Edition
Medical & Biological Engineering & Computing, Heidelberg, Springer Heidelberg, 2016, 0140-0118
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
30105 Physiology
Country of publisher
Germany
Confidentiality degree
není předmětem státního či obchodního tajemství
Impact factor
Impact factor: 1.916
RIV identification code
RIV/00216224:14110/16:00088865
Organization unit
Faculty of Medicine
UT WoS
000374470600005
Keywords in English
Ethanol; Cardiomyocyte; Action potential; Rat ventricular cell model; Human ventricular cell model
Tags
Tags
International impact, Reviewed
Změněno: 2/8/2016 14:00, Ing. Mgr. Věra Pospíšilíková
Abstract
V originále
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.
Links
| NT14301, research and development project |
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