The effect of suppressing sinus rhythm on initiation and maintenance of atrial fibrillation was studied in 17 thoraeotomized and artificially ventilated dogs. Atrial fibrillation was evoked by methacholine chloride applied to the right atrium followed by light mechanical stimulation. Episodes of fibrillation were compared before and after sinus rhythm had been suppressed by injection of absolute alcohol or concentrated sodium pentobarbital into the sinus node artery. Sixty-nine control episodes of atrial fibrillation lasting 6.00 ± 0.36 (SE) minutes were easily initiated while the heart was in sinus rhythm. The response to methacholine application plus mechanical stimulation depended on the type of escape rhythm obtained after suppression of sinus rhythm. In ten dogs with no sign of supra A-V junctional pacemaker activity, only 50$ of the attempts to initiate fibrillation were successful. The 26 episodes of atrial fibrillation observed in this group of animals lasted 0.65 ± 0.23 (SE) minutes. In seven other dogs, supra A-V junctional pacemaker activity persisted after injection into the sinus node artery. In these seven dogs, 60% of the attempts at initiating fibrillation were successful, and the 18 episodes of fibrillation lasted 4.44 ± 0.30 (SE) minutes. In dogs showing no supra A-V junctional pacemaker activity, a more sustained arrhythmia was obtained after recovery of sinus node activity or during electrical pacing of the right atrial appendage. These observations suggest that the sinus node participates in the mechanism of cholinergic atrial fibrillation and that an equivalent role can be played by a natural or artificial supra A-V junctional pacemaker.
ADDITIONAL KEY WORDSatrial pacemakers electrical pacing A-V junctional escape rhythms methacholine sinus node perfusion• The mechanism of atrial fibrillation is still poorly understood. Experimental studies (1-4) have emphasized the importance of cholinergic stimulation in initiating and sustaining this arrhythmia. This cholinergic fibrillating influence has been related to a shortening of the refractory period of atrial tissues, a faster rate of membrane repolarization and a variable degree of homogeneity in the excitability of atrial fibers (5-7). Whether pacemaker inhibition, also a cholinergic effect, plays aFrom the