The discontinuous nature of propagation in normal canine cardiac muscle. Evidence for recurrent discontinuities of intracellular resistance that affect the membrane currents.

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Abstract
When the propagation velocity of action potentials is modified by changing the internal resistance of a cell, cable theory predicts that the shape of the action potential upstroke should not change; changes in velocity associated with changes in the upstroke usually are attributed to changes in membrane properties. In normal cardiac muscle changes in the upstroke with velocity occur under conditions in which the membrane properties could not have changed. Propagation in atrial and ventricular muscle was studied in which the velocity of propagation was different at different angles with respect to the cell orientation. Fast upstrokes were associated with low propagation velocities (in a direction transverse to the long cell axis) and slower upstrokes were associated with high propagation velocities (in the direction of the long cell axis). Such changes in the shape of depolarization can be accounted for by the discrete cellular nature of cardiac muscle. The recurrent discontinuities in intracellular resistance cause propagation to be discontinuous on a microscopic scale. The presence of discontinuities in intracellular resistance reverses the usual association of high velocity and high safety factor for propagation: propagation at a low velocity is more resistant to disturbances in membrane properties than is propagation at a higher velocity. This inverted relationship suggested that propagation could continue in a direction transverse to the long axis of the cells when block occurs in the longitudinal direction, with resultant reentrant propagation. Such prediction was confirmed in the study of the propagation of premature action potentials in atrial muscle.