Metabolic impairment and potassium channel openers, such as pinacidil, activate the ATP-sensitive potassium current [IK(ATP)]. This effect leads to a reduction of action potential duration (APD), eliciting serious arrhythmias, and reentry. However, the arrhythmogenic effects of the activation of IK(ATP) should be further studied. Our goal is to simulate the effects of pinacidil on APD shortening with the aid of a computer model. This model is based on experimental results of the effects of pinacidil on IK(ATP) and its voltage dependence. The mathematical formulation completed the IK(ATP) model by Ferrero et al., which was introduced into the ventricular cardiac action potential model described by Luo and Rudy (phase II). The results of the simulations correlate well with experimentally estimated values and show that pinacidil strongly affects APD. Further simulations could elucidate the proarrhythmic or antiarrhythmic effects of pinacidil in myocardial tissue.
|Original language||English (US)|
|Number of pages||4|
|Journal||Computers in cardiology|
|State||Published - 1998|
ASJC Scopus subject areas
- Computer Science Applications
- Cardiology and Cardiovascular Medicine