Fox2002_IonicMechanism_CardiacMyocytes

This a model from the article:
Ionic mechanism of electrical alternans.

Fox JJ, McHarg JL, Gilmour RF Jr. Am J Physiol Heart Circ Physiol
2002 Feb;282(2):H516-30 11788399
,
Abstract:

Although alternans of action potential duration (APD) is a robust feature of the
rapidly paced canine ventricle, currently available ionic models of cardiac
myocytes do not recreate this phenomenon. To address this problem, we developed
a new ionic model using formulations of currents based on previous models and
recent experimental data. Compared with existing models, the inward rectifier
K(+) current (I(K1)) was decreased at depolarized potentials, the maximum
conductance and rectification of the rapid component of the delayed rectifier
K(+) current (I(Kr)) were increased, and I(Kr) activation kinetics were slowed.
The slow component of the delayed rectifier K(+) current (I(Ks)) was increased
in magnitude and activation shifted to less positive voltages, and the L-type
Ca(2+) current (I(Ca)) was modified to produce a smaller, more rapidly
inactivating current. Finally, a simplified form of intracellular calcium
dynamics was adopted. In this model, APD alternans occurred at cycle lengths =
150-210 ms, with a maximum alternans amplitude of 39 ms. APD alternans was
suppressed by decreasing I(Ca) magnitude or calcium-induced inactivation and by
increasing the magnitude of I(K1), I(Kr), or I(Ks). These results establish an
ionic basis for APD alternans, which should facilitate the development of
pharmacological approaches to eliminating alternans.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Fox JJ, McHarg JL, Gilmour RF Jr. (2002) - version02

The original CellML model was created by:
Noble, Penny,

[e-mail]
Oxford University
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