Acute effects of ethanol on action potential and intracellular Ca2+ transient in cardiac ventricular cells: a simulation study
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388998%3A_____%2F16%3A00453143" target="_blank" >RIV/61388998:_____/16:00453143 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216224:14110/16:00088865
Výsledek na webu
<a href="http://dx.doi.org/10.1007/s11517-015-1366-8" target="_blank" >http://dx.doi.org/10.1007/s11517-015-1366-8</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1007/s11517-015-1366-8" target="_blank" >10.1007/s11517-015-1366-8</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Acute effects of ethanol on action potential and intracellular Ca2+ transient in cardiac ventricular cells: a simulation study
Popis výsledku v původním jazyce
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 8 mM). These changes were almost exclusively caused by the ethanol-induced alterations of IK1. The cytosolic Ca2+ transient decreased gradually with the increasing ethanol concentration as a result of the ethanol-induced inhibition of ICa. In the human model, ethanol produced a dose-dependent APD lengthening, dominated by ethanol effect on IKr, the key repolarising current in human ventricles. This effect might contribute to the clinically observed proarrhythmic effects of ethanol in predisposed individuals.
Název v anglickém jazyce
Acute effects of ethanol on action potential and intracellular Ca2+ transient in cardiac ventricular cells: a simulation study
Popis výsledku anglicky
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 8 mM). These changes were almost exclusively caused by the ethanol-induced alterations of IK1. The cytosolic Ca2+ transient decreased gradually with the increasing ethanol concentration as a result of the ethanol-induced inhibition of ICa. In the human model, ethanol produced a dose-dependent APD lengthening, dominated by ethanol effect on IKr, the key repolarising current in human ventricles. This effect might contribute to the clinically observed proarrhythmic effects of ethanol in predisposed individuals.
Klasifikace
Druh
J<sub>x</sub> - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)
CEP obor
BO - Biofyzika
OECD FORD obor
—
Návaznosti výsledku
Projekt
<a href="/cs/project/NT14301" target="_blank" >NT14301: Vliv ethanolu a jeho metabolitu acetaldehydu na srdeční inward rectifier draslíkové proudy: vztah k fibrilaci síní po konzumaci alkoholu?</a><br>
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2016
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Medical & Biological Engineering & Computing
ISSN
0140-0118
e-ISSN
—
Svazek periodika
54
Číslo periodika v rámci svazku
5
Stát vydavatele periodika
DE - Spolková republika Německo
Počet stran výsledku
10
Strana od-do
753-762
Kód UT WoS článku
000374470600005
EID výsledku v databázi Scopus
2-s2.0-84939446301