ABSTRACT:
This a model from the article:
A novel computational model of the human ventricular action potential and Ca
transient.
Grandi E, Pasqualini FS, Bers DM. J Mol Cell Cardiol
2010 Jan;48(1):112-21 19835882
,
Abstract:
We have developed a detailed mathematical model for Ca handling and ionic
currents in the human ventricular myocyte. Our aims were to: (1) simulate basic
excitation-contraction coupling phenomena; (2) use realistic repolarizing K
current densities; (3) reach steady-state. The model relies on the framework of
the rabbit myocyte model previously developed by our group, with subsarcolemmal
and junctional compartments where ion channels sense higher [Ca] vs. bulk
cytosol. Ion channels and transporters have been modeled on the basis of the
most recent experimental data from human ventricular myocytes. Rapidly and
slowly inactivating components of I(to) have been formulated to differentiate
between endocardial and epicardial myocytes. Transmural gradients of Ca handling
proteins and Na pump were also simulated. The model has been validated against a
wide set of experimental data including action potential duration (APD)
adaptation and restitution, frequency-dependent increase in Ca transient peak
and [Na](i). Interestingly, Na accumulation at fast heart rate is a major
determinant of APD shortening, via outward shifts in Na pump and Na-Ca exchange
currents. We investigated the effects of blocking K currents on APD and
repolarization reserve: I(Ks) block does not affect the former and slightly
reduces the latter; I(K1) blockade modestly increases APD and more strongly
reduces repolarization reserve; I(Kr) blockers significantly prolong APD, an
effect exacerbated as pacing frequency is decreased, in good agreement with
experimental results in human myocytes. We conclude that this model provides a
useful framework to explore excitation-contraction coupling mechanisms and
repolarization abnormalities at the single myocyte level. Copyright 2009
Elsevier Inc. All rights reserved.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Grandi E, Pasqualini FS, Bers DM. (2009) - version=1.0
The original CellML model was created by:
Geoffrey Nunns
gnunns1@jhu.edu
The University of Auckland
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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.
Camille Laibe 
