Quantitative modelling of interaction of propafenone with
sodium channels in cardiac cells.

D 2001

Quantitative modelling of interaction of propafenone with sodium channels in cardiac cells.

PÁSEK, Michal a Jiří ŠIMURDA

Základní údaje

Originální název

Quantitative modelling of interaction of propafenone with sodium channels in cardiac cells.

Autoři

PÁSEK, Michal (203 Česká republika, garant) a Jiří ŠIMURDA (203 Česká republika)

Vydání

Pula (Croatia), Proceedings of the International Federation for Medical and Biologocal Engineering, s. 1028-1031, 2001

Nakladatel

Faculty of Electrical Engineering, Zagreb

Další údaje

Jazyk

angličtina

Typ výsledku

Stať ve sborníku

Obor

10610 Biophysics

Stát vydavatele

Chorvatsko

Utajení

není předmětem státního či obchodního tajemství

Kód RIV

RIV/00216224:14110/01:00005060

Organizační jednotka

Lékařská fakulta

ISBN

953-184-024-5

UT WoS

000176065600281

Klíčová slova anglicky

cardiac cell; propafenone; quantitative modelling

Štítky

Cardiac cell, propafenone, Quantitative modelling

Změněno: 25. 6. 2009 16:20, doc. Ing. Michal Pásek, Ph.D.

Anotace

V originále

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.

Citovat

PÁSEK, Michal a 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, s. 1028-1031. ISBN 953-184-024-5.

@inproceedings{383829,
   author = {Pásek, Michal and Šimurda, Jiří},
   address = {Pula (Croatia)},
   booktitle = {Proceedings of the International Federation for Medical and Biologocal Engineering},
   keywords = {cardiac cell; propafenone; quantitative modelling},
   language = {eng},
   location = {Pula (Croatia)},
   isbn = {953-184-024-5},
   pages = {1028-1031},
   publisher = {Faculty of Electrical Engineering, Zagreb},
   title = {Quantitative modelling of interaction of propafenone with sodium channels in cardiac cells.},
   year = {2001}
}

TY  - CONF
ID  - 383829
AU  - Pásek, Michal - Šimurda, Jiří
PY  - 2001
TI  - Quantitative modelling of interaction of propafenone with sodium channels in cardiac cells.
PB  - Faculty of Electrical Engineering, Zagreb
CY  - Pula (Croatia)
SN  - 9531840245
KW  - cardiac cell
KW  - propafenone
KW  - quantitative modelling
N2  - 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.
ER  -

PÁSEK, Michal a Jiří ŠIMURDA. Quantitative modelling of interaction of propafenone with sodium channels in cardiac cells. In \textit{Proceedings of the International Federation for Medical and Biologocal Engineering}. Pula (Croatia): Faculty of Electrical Engineering, Zagreb, 2001, s.~1028-1031. ISBN~953-184-024-5.

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