Abstract
Experiments have demonstrated that hypothermia prolongs action potential duration (APD) of myocytes. However, the effect of regional cooling on tissue responses to electrical stimulation is unknown. Methods: To develop a membrane model that reproduces the effects of cooling, equations representing temperature quotient Q10 dependence of membrane and gap-junctional currents were incorporated in the LRd model. Responses to both pacing and shocks at various temperatures were simulated in a 3×3-cm bidomain sheet with a 1-cm in diameter central region of cooling. Results: Lowering regional temperature from 37 to 32°C during pacing at 500 ms resulted in Q10 value of 2.0 for APD (166 vs. 235 ms) and of 1.3 for conduction velocity (CV) along fibers (58 vs. 50 cm/s). Further decrease in temperature to 27°C brought about higher Q10 (2.2 and 2.6 for APD and CV, respectively) and led to lower safety factor for propagation. At a temperature of 22°C, triggered activity was induced. Intriguingly, for regional cooling at below 32°C, a weak electric shock (6 V/cm) formed strong virtual electrodes (VEs; regions of positive and negative membrane polarization far from shock electrodes) around the cooled region border. Conclusion: While significant myocardial cooling causes arrhythmogenesis, shock-induced VEs formed in a weakly-cooled region may suggest a novel approach to low-energy defibrillation since the VEs underlie success of defibrillation and fibrillation control. [Jpn J Physiol 55 Suppl:S88 (2005)]
