Expanded model of the electric field hypothesis for propagation in cardiac muscle

Abstract

An electric field model for action potential (AP) propagation between adjoining myocardial cells has been further developed by expanding the model to a strand of 10 cells, increasing the number of active membrane segments per cell, incorporating Beeler-Reuter kinetics, assigning physiologically realistic values to the parameters, and employing a simpler numerical integration scheme. The major assumption is that the pre- and postjunctional membranes are excitable membranes. There is no requirement for a low-resistance coupling between the cells. The electric field that develops in the narrow junctional cleft between cells during the rising phase of the action potential in the prejunctional membrane acts to depolarize the postjunctional membrane to threshold. AP propagation occurred down the strand at a uniform velocity of 32 cm/sec under standard conditions. Propagation was found to be strongly dependent on radial cleft resistance ( R jc ) and the junctional membrane properties. There was an optimal R jc for maximum velocity under any given conditions. However, overall propagation velocity was determined by the AP conduction delay at the junctional clefts. K + accumulation in the clefts was shown to facilitate AP transmission. This model is consistent with many experimental facts concerning propagation in cardiac muscle, including discontinuous conduction, and suggests an alternative mechanism for AP propagation that does not depend on direct current flow between cells.