Lidocaine blocks Na, Ca and K currents of chick ventricular myocytes.

In addition to the well-known reduction in the maximal rate of rise the antiarrhythmic agent, lidocaine, also produces a shortening in the duration of the normal ventricular action potential. The voltage-dependent currents carried by Na, Ca and K ions were examined in the absence and presence of lidocaine, in order to identify the ionic mechanism(s) underlying the action potential shortening. Whole-cell and single channel currents were studied by the patch clamp method using single ventricular myocytes from embryonic chick hearts. Exposure to lidocaine (10 to 1000 microM) produced a decrease in the magnitude of the small-magnitude, slowly-inactivating component of the Na current, and a decrease in the magnitude of the Ca current; these results provide a mechanism for the action potential shortening and suggest possible explanations for the antiarrhythmic action of this therapeutic agent. A decrease in the magnitude of the inwardly-rectifying K+ current was also found, which was attributable to a reduction in the probability of opening of single K+ channels.