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

  1. 1.
    0453143 - ÚT 2017 RIV DE eng J - Článek v odborném periodiku
    Pásek, Michal - Bébarová, M. - Christé, G. - Šimurdová, M. - Šimurda, J.
    Acute effects of ethanol on action potential and intracellular Ca2+ transient in cardiac ventricular cells: a simulation study.
    Medical & Biological Engineering & Computing. Roč. 54, č. 5 (2016), s. 753-762. ISSN 0140-0118. E-ISSN 1741-0444
    Institucionální podpora: RVO:61388998
    Klíčová slova: ethanol * cardiomyocyte * action potential * rat ventricular cell model * human ventricular cell model
    Kód oboru RIV: BO - Biofyzika
    Impakt faktor: 1.916, rok: 2016

    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.
    Trvalý link: http://hdl.handle.net/11104/0265983

     
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