The influence of quinidine and procaine amide on myocardial contractility in vivo

Abstract

Quinidine and procaine amide were tested in experiments on dogs regarding their ability to alter myocardial contractility. Myocardial tension was measured directly by a strain gauge arch attached to the left ventricle in vivo. Both drugs in doses greater than 20 mg. per kg. depress contractility and their effects are similar on a weight basis. Considering that the therapeutic doses of procaine amide are generally larger than those of quinidine, the negative inotropic effect of the former is therapeutically more significant than that of the latter. The drugs altered the contractile tension curves in a characteristic manner so that both the peak contractile tension and the area under the tension-time curve were reduced. Reduction of the peak contractile tension to less than 40 per cent of its control value was found to be incompatible with subsequent recovery. Changes of a lesser magnitude were generally reversible. Administration of both drugs produced bradycardia and hypotension. The decrease in blood pressure followed the change of contractility. Both returned to control values during recovery. It is suggested that the negative inotropic effects of these drugs may be related to their known ability to increase the intracellular concentration of potassium in the myocardium.