Winslow, Rice, Jafri, Marban, O'Rorke, 1999
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.
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
|A schematic diagram describing the current flows across the cell membrane that are captured in the Winslow et al canine ventricular cell model.|