ABSTRACT:
This a model from the article:
Cardiac Ca2+ dynamics: the roles of ryanodine receptor adaptation and
sarcoplasmic reticulum load.
Jafri MS, Rice JJ, Winslow RL. Biophys J
1998 Mar;74(3):1149-68 9512016
,
Abstract:
We construct a detailed mathematical model for Ca2+ regulation in the
ventricular myocyte that includes novel descriptions of subcellular mechanisms
based on recent experimental findings: 1) the Keizer-Levine model for the
ryanodine receptor (RyR), which displays adaptation at elevated Ca2+; 2) a model
for the L-type Ca2+ channel that inactivates by mode switching; and 3) a
restricted subspace into which the RyRs and L-type Ca2+ channels empty and
interact via Ca2+. We add membrane currents from the Luo-Rudy Phase II
ventricular cell model to our description of Ca2+ handling to formulate a new
model for ventricular action potentials and Ca2+ regulation. The model can
simulate Ca2+ transients during an action potential similar to those seen
experimentally. The subspace [Ca2+] rises more rapidly and reaches a higher
level (10-30 microM) than the bulk myoplasmic Ca2+ (peak [Ca2+]i approximately 1
microM). Termination of sarcoplasmic reticulum (SR) Ca2+ release is
predominately due to emptying of the SR, but is influenced by RyR adaptation.
Because force generation is roughly proportional to peak myoplasmic Ca2+, we use
[Ca2+]i in the model to explore the effects of pacing rate on force generation.
The model reproduces transitions seen in force generation due to changes in
pacing that cannot be simulated by previous models. Simulation of such complex
phenomena requires an interplay of both RyR adaptation and the degree of SR Ca2+
loading. This model, therefore, shows improved behavior over existing models
that lack detailed descriptions of subcellular Ca2+ regulatory mechanisms.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Jafri MS, Rice JJ, Winslow RL. (1998) - version03
The original CellML model was created by:
Lloyd, Catherine, May
c.lloyd@aukland.ac.nz
The University of Auckland
The Bioengineering Institute
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Vijayalakshmi Chelliah 
