Cell and tissue responses to electric shocks

Aim: Existing models of myocardial membrane kinetics have not been able to reproduce the experimentally-observed negative bias in the asymmetry of transmembrane potential changes (ΔV_m) induced by strong electric shocks. The goals of this study are (1) to demonstrate that this negative bias could be reproduced by the addition, to the membrane model, of electroporation and an outward current, I_a, part of the K⁺ flow through the L-type Ca²⁺-channel, and (2) to determine how such modifications in the membrane model affect shock-induced break excitation in a 2D preparation. Methods and results: We conducted simulations of shocks in bidomain fibres and sheets with membrane dynamics represented by the Luo-Rudy dynamic model (LRd'2000), to which electroporation (LRd+EP model) and the outward current, I_a, activated upon strong shock-induced depolarization (aLRd model) was added. Assuming I_a is a part of K⁺ flow through the L-type Ca²⁺-channel enabled us to reproduce both the experimentally observed rectangularly-shaped positive ΔV_m and the value of near 2 of the negative-to-positive ΔV_m ratio. In the sheet, I_a not only contributed to the negative bias in ΔV_m asymmetry at sites polarized by physical and virtual electrodes, but also restricted positive ΔV_m. Electroporation, in its turn, was responsible for the decrease in cathode-break excitation threshold in the aLRd sheet, compared with the other two cases, as well as for the occurrence of the excitation after the shock-end rather than during the shock. Conclusions: The incorporation of electroporation and I_a in a membrane model ensures match between simulation results and experimental data. The use of the aLRd model results in a lower threshold for shock-induced break excitation.