Canine Ventricular Cell Model, 1999
Catherine
Lloyd
Bioengineering Institute, University of Auckland
Model Status
This model has been curated and unit-checked by Penny Noble and is known to run in PCEnv and COR to replicate the published results.
Model Structure
In 1999 Raimond Winslow, Jeremy Rice, Saleet Jafri, Eduardo Marban and Brian O'Rourke published a computational model of the action potential and of intracellular Ca2+ handling in normal and failing canine ventricular myocytes. Using the experimental data of O'Rourke et al (1999) they modified Jafri et al's guinea pig ventricular cell model (1999) to make it appropriate for canine midmyocardial cells (see the figure below). The CellML description here is of the normal canine ventricular myocyte model. In failing myocytes i_to1 and i_K1 are down regulated on average by 66 percent and 32 percent respectively. The kinetic properties of i_to1 and the gating behaviour if i_K1 remain unaltered. Only the number of expressed channels is reduced (the control may be pre- or post-transcriptional but it is not post-translational). On the basis of these data, the effects of terminal heart failure are modelled by reducing the peak conductance of i_to1 and i_K1. Downregulation of the sarcoplasmic reticulum Ca2+ pump is modelled by simultaneous scaling of both the forward and reverse maximum pump rates Vmaxf and Vmaxr by a scale factor KSR. Upregulation of the Na-Ca exchanger is modelled by increasing a scale factor KNaCa.
The complete original paper reference is cited below:
Mechanisms of Altered Excitation-Contraction Coupling in Canine Tachycardia-Induced Heart Failure, II Model Studies, Raimond L. Winslow, Jeremy Rice, Saleet Jafri, Eduardo Marban and Brian O'Rourke, 1999,
Circulation Research
, 84, 571-586. PubMed ID: 10082479
cell diagram of the Winslow et al ventricular cell model showing ionic currents, pumps and exchangers within the sarcolemma and the sarcoplasmic reticulum
A schematic diagram describing the current flows across the cell membrane that are captured in the Winslow et al canine ventricular cell model.
the cellml rendering of the Winslow et al model
Department of Physiology, Anatomy & Genetics, University of Oxford
keyword
heart failure
ventricular myocyte
excitation-contraction coupling
canine
calcium dynamics
Ventricular Myocyte
electrophysiology
cardiac
tachycardia
Catherine Lloyd
10
50000
0.001
bdf15
M
Jafri
S
Raimond
Winslow
L
2007-10-30T11:32:02+13:00
James
Lawson
Richard
This model has been curated by Penny Noble and is known to run in PCEnv and COR. It is able to produce the results of the model published in the Matsuoka 2003 paper but still contains some unit discrepancies.
Circulation Research
A multiple stimulus protocol component has been added to this model to allow simulations of trains of action potentials. Several variables have also been given cmeta:ids to allow them to be referenced in a PCEnv session file.
2006-05-15T00:00:00+00:00
penny.noble@dpag.ox.ac.uk
Penny
Noble
J
1999-03-19 00:00
units checked, curated
John
Rice
J
Penny
Noble
J
Eduardo
Marban
Oxford University
Department of Physiology, Anatomy & Genetics
2008-02-25T12:32:09+13:00
This is the CellML description of Winslow et al's mathematical model of ionic fluxes and Ca regulation in normal and failing ventricular myocytes. This model is derived from Jafri et al's guinea pig ventricular model (1998) with modifications to better represent the conditions in a canine midmyocardial ventricular cell.
James Lawson
10082479
Brian
O'Rorke
Mechanisms of Altered Excitation-Contraction Coupling in Canine Tachycardia-Induced Heart Failure, II Model Studies
84
571
586