![]() |
|
|
1 Department of Pharmacology, Cornell University Medical College, New York, New York
The sensitivity of atrial and ventricular pacemakers to the depressant actions of quinidine was determined in isolated cat hearts with surgically induced heart block. Quinidine administered by single injection or by perfusion caused a greater slowing of the atrial rate than of the ventricular rate. The greater sensitivity of the atrial pacemaker to quinidine was also indicated by the finding that the ventricular pacemaker completely recovered from quinidine depression while the atrial pacemaker failed to recover fully. There was also a greater incidence of rhythm disturbances in the atrium than in the ventricle. It may be possible to explain the greater sensitivity of the atrial pacemaker to quinidine depression by the fact that its rate of firing is greater than that of the ventricle. A faster rate of firing of an abnormal focus may also explain, at least in part, the observation that ventricular tachycardia can be successfully converted to normal sinus rhythm by quinidine. Regardless of the method of administration or the concentration used, quinidine did not accelerate the atrial or ventricular rate. This suggested that the accleration of the heart rate by quinidine in vivo depends on an intact sympathetic nervous system.
Accepted on October 19, 1965