current-voltage relationships in long Purkinje fibers was corrected for cable complications or when experiments were done in short Purkinje fibers. To minimize complications due to membrane rectifier properties, GK was measured using intracellular application of small hyperpolarizing current pulses as Vm was decreased from -90 to -60 mv by increasing the [K]0 from 3 to 15 mM before and after lidocaine. Lidocaine increased the GK over this range of Vm.These results suggest that lidocaine increases membrane potassium conductance within the range of Vm where the pacemaker potential is seen, an action which can account for its ability to suppress automaticity, and, in part, for its ability to prevent reentrant arrhythmias. INTRODUCTIONThe efficacy of lidocaine hydrochloride in the treatment of cardiac ventricular arrhythmias after open heart surgery, myocardial infarction, and digitalis has been established and recently reviewed (1). Electrophysiologic investigations have shown that in cardiac Purkinje fibers, lidocaine: (a) shortens the action potential duration and decreases the effective refractory period, and (b) exerts an antiautomatic effect by decreasing the slope of slow diastolic depolarization without affecting the maximum diastolic transmembrane voltage (2-4). These observations led Bigger and Mandel to postulate that lidocaine may increase potassium conductance in mammalian cardiac Purkinje fibers (3). The present experiments were designed to test this hypothesis in sheep Purkinje fibers using microelectrode techniques. The effects of lidocaine in a concentration equivalent to clinical plasma antiarrhythmic levels on the transmembrane voltage and on current-voltage relationships suggest that lidocaine does increase potassium conductance in Purkinje fibers.