Rate Dependence and Regulation of Action Potential and Calcium Transient in a Ventricular Cell Model. Based on the Hund-Rudy 2004 model. Imported from the CellML version of the model.

Description

  In the paper described here, Thomas Hund and Yoram Rudy present
  a detailed, and physiologically realistic, mathematical model
  of a canine ventricular cell. Model simulations are able to
  recreate the rate-dependent phenomena associated with ion-channel
  kinetics, action potential properties, and calcium ion handling.
  The model is based on an epicardial myocyte because these cells
  contain the largest transient outward potassium current (when
  compared with endocardial or midmyocardial myocytes). The calcium/calmodulin-dependent
  protein kinase (CaMKII) regulatory pathway was embedded within
  the electrophysiological model, incorporating calcium-release
  formulation, calcium subspace, and dynamic chloride handling.
  Results from the model simulations revealed CaMKII is an important
  determinant of the rate dependence of the calcium transient,
  but not of the action potential duration, which depends instead
  on the ion-channel kinetics.

 
 * Original CellML note:
 * This CellML version of the model has been checked in COR and
 * OpenCell. The units are consistent and the model runs to recreate
 * the published results. This is the tissue version of the model,
 * to use this model embedded within tissue, set the initial
 * value of the variable tissue in component Environment to 1.

Figure: Action potential at steady-state for different action potential cycle lengths of 300, 600, and 900 ms.

Equations

The equations for this model may be viewed by running the JSim model applet and clicking on the Source tab at the bottom left of JSim's Run Time graphical user interface. The equations are written in JSim's Mathematical Modeling Language (MML). See the Introduction to MML and the MML Reference Manual. Additional documentation for MML can be found by using the search option at the Physiome home page.