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 (DeltaV(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 Ca(2+)-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 Ca(2+)-channel enabled us to reproduce both the experimentally observed rectangularly-shaped positive DeltaV(m) and the value of near 2 of the negative-to-positive DeltaV(m) ratio. In the sheet, I(a) not only contributed to the negative bias in DeltaV(m) asymmetry at sites polarized by physical and virtual electrodes, but also restricted positive DeltaV(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.