The role of spatial interactions in creating the dispersion of transmembrane potential by premature electric shocks.
Strong electric shocks applied during the refractory period can initiate or terminate cardiac arrhythmias. To elucidate the underlying mechanism, Knisley et al. used rabbit papillary muscle in vitro to scan the refractory period of an action potential with shocks of different strengths. The resulting map of the shock-induced changes in the transmembrane potential (Vm) illustrates the substrate for the creation of rotors. Our study uses computer simulations to reproduce this experimental map. Three models (a space-clamped membrane, a single cell, and a one-dimensional fiber) were used to determine whether the observed map was caused by (i) the intrinsic dynamics of the membrane, (ii) the simultaneous depolarization and hyperpolarization of the opposite ends of each cell, or (iii) spatial interactions involving the whole muscle strand. The results show that the membrane and single cell models cannot reproduce the experimental map. The fiber model reproduces the shock-induced changes in Vm and demonstrates that they are caused by a propagating disturbance, which, depending on the coupling interval and the shock strength, can be a new action potential or an electrotonus and can arrive from the depolarized end or from both depolarized and hyperpolarized ends of the fiber. These results indicate that the induction of rotors in the heart may not be a direct effect of the electric field.
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