Quinidine in therapeutic doses significantly reduced heart rate, aortic pressure, and flow in anesthetized dogs, but did not directly affect myocardial contractility.
Does quinidine directly affect myocardial contractility in anesthetized mongrel dogs?
Quinidine does not directly depress myocardial contractility at therapeutic doses, suggesting that previously reported adverse cardiac effects may be due to toxic doses or peripheral circulatory effects.
Since quinidine is one of the few agents available to treat and prevent ventricular arrhythmias in ambulatory patients, its hemodynamic effects have been reevaluated. When given in therapeutic doses to anesthetized mongrel dogs, quinidine significantly reduced heart rate, aortic pressure and flow, but it did not significantly change the first derivative of the left ventricular pressure curve (left ventricular dp/dt) in nine dogs. A subsequent group of dogs was studied after vagotomy and practolol administration to block cardiac reflexes. This group showed significant reductions in heart rate, aortic pressure and left ventricular dp/dt, with the latter returning to predrug control values when preload, afterload and heart rate were maintained constant. These studies suggest that quinidine does not directly affect myocardial contractility when given in therapeutic doses. Furthermore, the reduction in heart rate in these animals provides support for a direct depressant effect of quinidine on the sinus node. The adverse effects of quinidine on cardiac function previously reported may be due to the use of toxic doses or are secondary to quinidine peripheral circulatory effects, rather than due to a direct reduction in cardiac contractile state.
Markiewicz et al. (Thu,) reported a other. Quinidine vs. Predrug control values was evaluated on Hemodynamic effects including heart rate, aortic pressure and flow, and left ventricular dp/dt. Quinidine in therapeutic doses significantly reduced heart rate, aortic pressure, and flow in anesthetized dogs, but did not directly affect myocardial contractility.