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MODEL0406270966 - Livshitz2007_CardiacMyocytes

 

The following model is part of the non-curated branch of BioModels Database. While the syntax of the model has been verified, its semantics remains unchecked. Any annotation present in the models is not a product of BioModels' annotators. We are doing our best to incorporate this model into the curated branch as soon as possible. In the meantime, we display only limited metadata here. For further information about the model, please download the SBML file.


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Reference Publication
Publication ID: 17277017
Livshitz LM, Rudy Y.
Regulation of Ca2+ and electrical alternans in cardiac myocytes: role of CAMKII and repolarizing currents.
Am. J. Physiol. Heart Circ. Physiol. 2007 Jun; 292(6): H2854-66
Cardiac Bioelectricity and Arrhythmia Center, Washington University in St. Louis, Missouri 63130-4899, USA.  [more]
Model
Original Model: CellML logo
Submitter: Vijayalakshmi Chelliah
Submission Date: 22 Apr 2009 17:59:58 UTC
Last Modification Date: 22 Apr 2009 17:59:58 UTC
Creation Date: 22 Apr 2009 17:59:58 UTC
Encoders:
bqmodel:isDerivedFrom PubMed 10777735
PubMed 7514509
PubMed 15505083
bqbiol:occursIn Brenda Tissue Ontology cardiac muscle fiber
bqbiol:hasTaxon Taxonomy Canis lupus familiaris
Taxonomy Cavia porcellus
bqbiol:isVersionOf Gene Ontology membrane repolarization during ventricular cardiac muscle cell action potential
Notes

This a model from the article:
Regulation of Ca2+ and electrical alternans in cardiac myocytes: role of CAMKII and repolarizing currents.
Livshitz LM, Rudy Y. Am J Physiol Heart Circ Physiol. 2007 Jun;292(6):H2854-66. 17277017 ,
Abstract:
Alternans of cardiac repolarization is associated with arrhythmias and sudden death. At the cellular level, alternans involves beat-to-beat oscillation of the action potential (AP) and possibly Ca(2+) transient (CaT). Because of experimental difficulty in independently controlling the Ca(2+) and electrical subsystems, mathematical modeling provides additional insights into mechanisms and causality. Pacing protocols were conducted in a canine ventricular myocyte model with the following results: 1) CaT alternans results from refractoriness of the sarcoplasmic reticulum Ca(2+) release system; alternation of the L-type calcium current has a negligible effect; 2) CaT-AP coupling during late AP occurs through the sodium-calcium exchanger and underlies AP duration (APD) alternans; 3) increased Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) activity extends the range of CaT and APD alternans to slower frequencies and increases alternans magnitude; its decrease suppresses CaT and APD alternans, exerting an antiarrhythmic effect; and 4) increase of the rapid delayed rectifier current (I(Kr)) also suppresses APD alternans but without suppressing CaT alternans. Thus CaMKII inhibition eliminates APD alternans by eliminating its cause (CaT alternans) while I(Kr) enhancement does so by weakening CaT-APD coupling. The simulations identify combined CaMKII inhibition and I(Kr) enhancement as a possible antiarrhythmic intervention.

This model was taken from the CellML repository and automatically converted to SBML.
The original model was: Livshitz LM, Rudy Y. (2007) - version01
The original CellML model was created by:
Noble, Penny,
penny.noble@dpag.ox.ac.uk
The University of Oxford

This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
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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.

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