BioModelsapplication/xmlhttps://www.ebi.ac.uk/biomodels/model/download/MODEL1006230048?filename=MODEL1006230048.pdfhttps://www.ebi.ac.uk/biomodels/model/download/MODEL1006230048?filename=MODEL1006230048-biopax2.owlhttps://www.ebi.ac.uk/biomodels/model/download/MODEL1006230048?filename=MODEL1006230048-biopax3.owlhttps://www.ebi.ac.uk/biomodels/model/download/MODEL1006230048?filename=MODEL1006230048_url.xmlhttps://www.ebi.ac.uk/biomodels/model/download/MODEL1006230048?filename=MODEL1006230048_urn.xmlhttps://www.ebi.ac.uk/biomodels/model/download/MODEL1006230048?filename=MODEL1006230048.scihttps://www.ebi.ac.uk/biomodels/model/download/MODEL1006230048?filename=MODEL1006230048.pnghttps://www.ebi.ac.uk/biomodels/model/download/MODEL1006230048?filename=MODEL1006230048.xpphttps://www.ebi.ac.uk/biomodels/model/download/MODEL1006230048?filename=MODEL1006230048.vcmlhttps://www.ebi.ac.uk/biomodels/model/download/MODEL1006230048?filename=MODEL1006230048.mprimaryOK200Camille LaibeNon-curatedordinary differential equation modelL2V4https://www.ebi.ac.uk/biomodels/MODEL100623004818160660falseBioModelsSBMLModelsMahajan2008 CardiacActionPotential Arrhythmias2008MODEL1006230048Aman Mahajan, Yohannes Shiferaw, Daisuke Sato, Ali Baher, Riccardo Olcese, Lai-Hua Xie, Ming-Jim Yang, Peng-Sheng Chen, Juan G Restrepo, Alain Karma, Alan Garfinkel, Zhilin Qu, James N WeissAman Mahajan18160660,
Mathematical modeling of the cardiac action potential has proven to be a powerful tool for illuminating various aspects of cardiac function, including cardiac arrhythmias. However, no currently available detailed action potential model accurately reproduces the dynamics of the cardiac action potential and intracellular calcium (Ca(i)) cycling at rapid heart rates relevant to ventricular tachycardia and fibrillation. The aim of this study was to develop such a model. Using an existing rabbit ventricular action potential model, we modified the L-type calcium (Ca) current (I(Ca,L)) and Ca(i) cycling formulations based on new experimental patch-clamp data obtained in isolated rabbit ventricular myocytes, using the perforated patch configuration at 35-37 degrees C. Incorporating a minimal seven-state Markovian model of I(Ca,L) that reproduced Ca- and voltage-dependent kinetics in combination with our previously published dynamic Ca(i) cycling model, the new model replicates experimentally observed action potential duration and Ca(i) transient alternans at rapid heart rates, and accurately reproduces experimental action potential duration restitution curves obtained by either dynamic or S1S2 pacing.. 2, 94.
UCLA Cardiovascular Research Laboratory, Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine at UCLA, Los Angeles, California, USA.laibe@ebi.ac.ukEMBL-EBIMathematical modeling of the cardiac action potential has proven to be a powerful tool for illuminating various aspects of cardiac function, including cardiac arrhythmias. However, no currently available detailed action potential model accurately reproduces the dynamics of the cardiac action potential and intracellular calcium (Ca(i)) cycling at rapid heart rates relevant to ventricular tachycardia and fibrillation. The aim of this study was to develop such a model. Using an existing rabbit ventricular action potential model, we modified the L-type calcium (Ca) current (I(Ca,L)) and Ca(i) cycling formulations based on new experimental patch-clamp data obtained in isolated rabbit ventricular myocytes, using the perforated patch configuration at 35-37 degrees C. Incorporating a minimal seven-state Markovian model of I(Ca,L) that reproduced Ca- and voltage-dependent kinetics in combination with our previously published dynamic Ca(i) cycling model, the new model replicates experimentally observed action potential duration and Ca(i) transient alternans at rapid heart rates, and accurately reproduces experimental action potential duration restitution curves obtained by either dynamic or S1S2 pacing.A rabbit ventricular action potential model replicating cardiac dynamics at rapid heart rates.Mahajan Aman A, Shiferaw Yohannes Y, Sato Daisuke D, Baher Ali A, Olcese Riccardo R, Xie Lai-Hua LH, Yang Ming-Jim MJ, Chen Peng-Sheng PS, Restrepo Juan G JG, Karma Alain A, Garfinkel Alan A, Qu Zhilin Z, Weiss James N JNfalseMahajan2008_CardiacActionPotential_Arrhythmias
This a model from the article:
A rabbit ventricular action potential model replicating cardiac dynamics at
rapid heart rates.
Mahajan A, Shiferaw Y, Sato D, Baher A, Olcese R, Xie LH, Yang MJ, Chen PS,
Restrepo JG, Karma A, Garfinkel A, Qu Z, Weiss JN. Biophys J
2008 Jan 15;94(2):392-410 18160660
,
Abstract:
Mathematical modeling of the cardiac action potential has proven to be a
powerful tool for illuminating various aspects of cardiac function, including
cardiac arrhythmias. However, no currently available detailed action potential
model accurately reproduces the dynamics of the cardiac action potential and
intracellular calcium (Ca(i)) cycling at rapid heart rates relevant to
ventricular tachycardia and fibrillation. The aim of this study was to develop
such a model. Using an existing rabbit ventricular action potential model, we
modified the L-type calcium (Ca) current (I(Ca,L)) and Ca(i) cycling
formulations based on new experimental patch-clamp data obtained in isolated
rabbit ventricular myocytes, using the perforated patch configuration at 35-37
degrees C. Incorporating a minimal seven-state Markovian model of I(Ca,L) that
reproduced Ca- and voltage-dependent kinetics in combination with our previously
published dynamic Ca(i) cycling model, the new model replicates experimentally
observed action potential duration and Ca(i) transient alternans at rapid heart
rates, and accurately reproduces experimental action potential duration
restitution curves obtained by either dynamic or S1S2 pacing.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Mahajan A, Shiferaw Y, Sato D, Baher A, Olcese R, Xie LH, Yang MJ, Chen PS,
Restrepo JG, Karma A, Garfinkel A, Qu Z, Weiss JN. (2008) - version=1.0
The original CellML model was created by:
Penny Noble
penny.noble@dpag.ox.ac.uk
The University of Oxford
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To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2012-02-022005-01-012010-06-23MODEL100623004818160660MODEL1006230048GO:00860019986BTO:0002320