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The effects of selected drugs on the sustained atrial flutter induced in conscious dogs with surgically produced right atrial enlargement (TI dogs) were evaluated. This was done to better understand the electrophysiologic mechanism of the tachyarrhythmias. Agents known to cause a slowing of atrioventricular (AV) nodal conduction--verapamil, methacholine, and phenylephrine--did not significantly decrease the rate of the induced flutter, whereas beta-adrenergic stimulation with an infusion of isoproterenol increased the rate of the flutter in all trials. Propranolol and atropine had little effect on the atrial flutter rate. Agents known to increase atrial refractoriness, such as procainamide, n-acetylprocainamide, bretylium, and clofilium, all increased the cycle length of the induced flutter and, in some cases, terminated the arrhythmia. These results suggest then that the perpetuation of the sustained atrial flutter in the conscious TI dog is not due to a delayed afterdepolarization mechanism but is more likely due to reentrant excitation. Furthermore, it is unlikely that the flutter is due to reentry over a pathway involving the AV node; rather, the arrhythmia seems to be caused by reentrant excitation of the leading circle type.
Penelope A. Boyden (Wed,) studied this question.