PÁSEK, Michal and Jiří ŠIMURDA. Quantitative modelling of interaction of propafenone with sodium channels in cardiac cells. In Proceedings of the International Federation for Medical and Biologocal Engineering. Pula (Croatia): Faculty of Electrical Engineering, Zagreb, 2001, p. 1028-1031. ISBN 953-184-024-5.
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Basic information
Original name Quantitative modelling of interaction of propafenone with sodium channels in cardiac cells.
Authors PÁSEK, Michal (203 Czech Republic, guarantor) and Jiří ŠIMURDA (203 Czech Republic).
Edition Pula (Croatia), Proceedings of the International Federation for Medical and Biologocal Engineering, p. 1028-1031, 2001.
Publisher Faculty of Electrical Engineering, Zagreb
Other information
Original language English
Type of outcome Proceedings paper
Field of Study 10610 Biophysics
Country of publisher Croatia
Confidentiality degree is not subject to a state or trade secret
RIV identification code RIV/00216224:14110/01:00005060
Organization unit Faculty of Medicine
ISBN 953-184-024-5
UT WoS 000176065600281
Keywords in English cardiac cell; propafenone; quantitative modelling
Tags Cardiac cell, propafenone, Quantitative modelling
Changed by Changed by: doc. Ing. Michal Pásek, Ph.D., učo 46541. Changed: 25/6/2009 16:20.
Abstract
A mathematical model of the interaction of propafenone with sodium channels is based on experimental data that demonstrate use dependent effect of the drug. Transitions among channel states are described by a kinetic diagram and a corre-sponding set of differential equations. The values of rate constants of the drug-receptor reaction are fitted to experimental data by repeated computer simulations using a genetic algorithm. The model suggests the following interpretation of the obtained experimental results: 1) The affinity of the drug to its binding site is high in the open and inactivated states while it is low in the resting state. 2) The biphasic development of the block during depolarization is consistent with a high association rate constant in the open state and a lower one in the inactivated state. 3) The observed double exponential time course of recovery of INa at resting voltage after depolarizing pulse may result from concurrent drug release from inactivated and non-inactivated blocked channels.
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