Reassessment of the electrophysiological effects of the antiarrhythmic agent quinidine in canine Purkinje fibers

Microelectrode techniques were used to re-examine the direct effects of quinidine on isolated canine Purkinje fibers. Our results confirmed the previous findings that quinidine in a dose-related manner suppressed spontaneous activity, prolonged effective refractory period and depressed the maximal rate of upstroke (dv/dt). Quinidine shifted the membrane response curves to the right of the voltage axis regardless of external K⁺ concentrations. The drug diminished the phase 2 plateau of the action potential indicating a possible inhibitory effect on calcium influx. Quinidine generally lengthened the action potential duration (ADP) but the extent of the increase varied with the site of recording along the Purkinje conduction system. The shorter APDs were lengthened far more than the longer APDs, thus dissimilar APDs became more uniform. Following the alteration of external K⁺ between 2 mM and 6 mM, the effects of quinidine on transmembrane characteristics, including the depression of dv/dt, remain constant with the exception of APD.