An ionic model of the ventricular cell based on voltage-clamp and action potential data measured experimentally in dog heart has been developed. The model is used to test the hypothesis that spatial variation of the magnitude of Ito1, IK3, Ito2, and the recovery time constant of Ito1 reported in the literature can account for differences in action potential shape of epicardial (EPI), midmyocardial (M), and endocardial (ENDO) cells. The model results demonstrate that experimentally observed differences in EPI, M, and ENDO cells, that are phase 1 spike, notch, phase 3 repolarizaiion, and rate dependence (0.5-2Hz) of action potential duration (APD), are accounted for by the model. The simulated effects of blocking IK3 IKr and Ito1 also agree with experimental data in M cells. Reduction of Ito1, IK1 and Iup current magnitudes and increase of INaca produce prolongation of the APD in the model similar to that observed during pacing tachycardia-induced heart failure in dogs.
|Original language||English (US)|
|Number of pages||4|
|Journal||Computers in Cardiology|
|Publication status||Published - Dec 1 1996|
ASJC Scopus subject areas
- Computer Science Applications
- Cardiology and Cardiovascular Medicine