COMPUTER SIMULATION OF THE INTRACELLULAR MECHANISM OF THE CARDIAC ARRHYTHMIA CREATION AND SUPPRESSION
We consider a stochastic model of the ion dynamics of the pacemaker's heart cell based in the generalized Maltsev-Lakatta model of two oscillators including the electron-conformational model of ryanodine receptors. It is shown that the formation of the action potential significantly depends on the nature of interactions between the external membrane and intracellular (“Ca2+ clock”) oscillators. The constructive interaction between oscillators leads to the formation of a stable action potential, while a destructive interaction leads to parasitic effects, in particular, arrhythmias. We examined the influence of the model parameters characteristic of the rabbit sinoatrial heart node on the qualitative aspect of the time dependence of the cell membrane potential. The conditions under which spontaneous transition of oscillations to the abnormally fast mode occurs have been found and this mechanism has been described, thereby the behavior of the pacemaker cell during tachycardia has actually been modeled. Computer simulation shows that the suppression of fast potassium current normalizes the oscillatory mode of the ion dynamics of the pacemaker cell, that corresponds to the action of class III antiarrhythmic drugs.