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MODEL7814665196 - Wang2008_Neonatal_heartfunction


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Reference Publication
Publication ID: 18408122
Wang LJ, Sobie EA.
Mathematical model of the neonatal mouse ventricular action potential.
Am. J. Physiol. Heart Circ. Physiol. 2008 Jun; 294(6): H2565-75
Department of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine, New York, New York, USA.  [more]
Original Model: CellML logo
Submitter: Vijayalakshmi Chelliah
Submission Date: 23 Mar 2009 16:32:55 UTC
Last Modification Date: 03 Jun 2009 12:40:42 UTC
Creation Date: 23 Mar 2009 16:32:55 UTC
bqbiol:occursIn Brenda Tissue Ontology sinus node
bqbiol:hasTaxon Taxonomy Oryctolagus cuniculus
bqbiol:isVersionOf Gene Ontology ventricular cardiac muscle cell action potential
Human Disease Ontology heart disease
bqmodel:isDerivedFrom PubMed 15142845

This a model from the article:
Mathematical model of the neonatal mouse ventricular action potential.
Wang LJ, Sobie EA. Am J Physiol Heart Circ Physiol. (2008) 294(6) pp H2565-75; 18408122 ,
Therapies for heart disease are based largely on our understanding of the adult myocardium. The dramatic differences in action potential (AP) shape between neonatal and adult cardiac myocytes, however, indicate that a different set of molecular interactions in neonatal myocytes necessitates different treatment for newborns. Computational modeling is useful for synthesizing data to determine how interactions between components lead to systems-level behavior, but this technique has not been used extensively to study neonatal heart cell function. We created a mathematical model of the neonatal (day 1) mouse myocyte by modifying, on the basis of experimental data, the densities and/or formulations of ion transport mechanisms in an adult cell model. The new model reproduces the characteristic AP shape of neonatal cells, with a brief plateau phase and longer duration than the adult (action potential duration at 80% repolarization = 60.1 vs. 12.6 ms). The simulation results are consistent with experimental data, including 1) decreased density and altered inactivation of transient outward K+ currents, 2) increased delayed rectifier K+ currents, 3) Ca2+ entry through T-type as well as L-type Ca2+ channels, 4) increased Ca2+ influx through Na+/Ca2+ exchange, and 5) Ca2+ transients resulting from transmembrane Ca2+ entry rather than release from the sarcoplasmic reticulum (SR). Simulations performed with the model generated novel predictions, including increased SR Ca2+ leak and elevated intracellular Na+ concentration in neonatal compared with adult myocytes. This new model can therefore be used for testing hypotheses and obtaining a better quantitative understanding of differences between neonatal and adult physiology.

This model was taken from the CellML repository and automatically converted to SBML.
The original model was: Wang_Sobie 2008, version01
The original CellML model was created by:
Lloyd, Catherine, May
The University of Auckland
Auckland Bioengineering Institute

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