Noble, Varghese, Kohl, Noble, 1998

Model Status

This version has been curated and unit checked by Penny Noble and is known to run into COR and PCEnv. This variant is parameterised for the BASIC model, excluding acetylcholine dependent modulation and electromechanical processes. This model is also associated with a PCEnv session file.

Model Structure

In their 1998 paper, Denis Noble, Anthony Varghese, Peter Kohl and Penny Noble extended the guinea-pig ventricular cell model (originally developed in 1991 by Noble et al) to include accumulation and depletion of calcium in a diadic space between the sarcolemma and the sarcoplasmic reticulum, where the majority of calcium-induced calcium release is triggered. The model also includes rapid (i_Kr) and slow (i_Ks) components of the delayed rectifier current, and length- and tension-dependent changes in mechanical and electrophysiological processes have been incorporated (see the figure below). Drug-receptor interactions have also started to be modeled using the sodium channel as an example. The drugs used have the effect of blocking the inactivation h-gate of the fast sodium channel.

The complete original paper reference is cited below:

Improved guinea-pig ventricular cell model incorporating a diadic space, I_Kr and I_Ks, and length- and tension-dependent processes, Denis Noble, Anthony Varghese, Peter Kohl and Penelope Noble, 1998, Can J Cardiol , 14, 123-134. PubMed ID: 9487284

The raw CellML description of the Noble'98 model can be downloaded in various formats as described in . For an example of a more complete documentation for an electrophysiological model, see The Hodgkin-Huxley Squid Axon Model, 1952.

A schematic diagram describing the current flows across the cell membrane that are captured in the Noble'98 model.