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1 Cedars-Sinai Medical Research Institute, and the Division of Medicine, Cedars-Sinai Medical Center, Los Angeles, and the Department of Medicine, University of California, Los Angeles, California
The effects of quinidine on the canine heart were investigated in situ. In the anesthetized dog, the i.v. injection of quinidine sulfate causes prolongations of the RR, PQ, QRS and QT interval in surface electrograms. Intracellular potentials were recorded from the left ventricle. Quinidine causes a slight but significant prolongation of the duration of the membrane action potential. It causes a great decrease in the upstroke velocity of the membrane action potential. There are insignificant changes in the magnitudes of the membrane action potential, membrane resting potential and overshoot. The prolongation of the QRS duration in surface electrograms is associated with the decrease in the upstroke velocity of the membrane action potential. The prolongation of the QT interval corresponds to the prolongation of the duration of the membrane action potential. The prolongation in the duration of the membrane action potential and the decrease in the upstroke velocity prolong the effective refractory period. The prolongation of the effective refractory period and the decrease of the automaticity may be considered to be antiarrhythmic actions of quinidine.
Submitted on February 13, 1967
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