Role of slow inward current in the genesis of ventricular arrhythmia.

Action potentials of premature beats in ventricular muscle fibers showed a transient prolongation of duration as well as an increase in second depolarization of the plateau phase when the preceding diastolic intervals were progressively shortened. These changes were abolished by manganese ions. Voltage clamp experiments also disclosed a transient increase in slow inward current in premature excitations, of which time course was very similar to that in action potential changes. These results suggested that prolongation of action potential durations was mainly brought about by changes in slow inward current and this was partly related to the characteristics of recovery from inactivation of this current. An increase of slow inward current produced depressed conduction on the subsequent beat and it also shared the effects to extend the areas of slow response. These effects may accelerate the occurrence of re-entry.