Cardiovascular effects of quinidine and procainamide on intact dogs and isolated cross-perfused canine atria.

Abstract

The effects of quinidine and procainamide were studied in isolated canine atria cross-perfused with heparinized arterial blood from donor dogs as well as in these donor dogs. When administered intravenously to donor dogs, both drugs produced dose-related hypotensive effects, but quinidine was 3-10 times more potent than procainamide. Quinidine frequently caused tachycardia in the donor dogs, while procainamide usually produced bradycardia. Quinidine-induced tachycardia was partially suppressed by vagotomy and completely inhibited or changed to bradycardia after propranolol. In isolated atria, small doses of drugs caused slight negative chronotropic and inotropic effects, frequently accompanied by small and short-lasting increases in contractile force and heart rate. Only decreases in contractile force and rate were observed with large doses. Administration of quinidine and procainamide into the sinus node artery of the isolated atrium induced negative, biphasic, or triphasic changes in chronotropism and inotropism. In isolated atria, quinidine and verapamil depressed the contractile force to a greater extent at higher stimulation frequencies. Procainamide showed less of this effect, because atrial muscle became unresponsive to high-frequency pacing with the larger doses of procainamide. These results suggest that quinidine and procainamide have both cardiac-depressant and -stimulating properties.