Electrophysiological study of human ventricular heart muscle treated with quinidine: interaction with isoprenaline.

We have investigated the effects of quinidine on the force of contraction and the intracellularly recorded action potential in papillary muscles isolated from human hearts. All preparations were obtained from patients undergoing corrective open heart surgery. The following results were obtained: (1) quinidine had a depressant effect on myocardial contractile force; (2) quinidine reduced the maximal upstroke velocity of the action potential; (3) quinidine shortened the plateau phase and prolonged the terminal repolarization of the action potential; (4) at higher concentrations quinidine reduced the resting potential; and (5) the depression by quinidine of both the plateau and the force of contraction was antagonized by isoprenaline. It is concluded that quinidine reduces the membrane conductances for sodium, calcium, and potassium ions. All of these actions of quinidine may contribute to the antiarrhythmic effects of the drug. The negative inotropic effect of quinidine can be explained by a depression of the calcium conductance at the myocardial cell membrane. The results show that earlier findings in laboratory animals regarding the effects of quinidine on the upstroke velocity and repolarization phase of the action potential are applicable to the human heart.