A possible mechanism of the antiarrhythmic action of glucagon

The effects of glucagon on ouabain-induced ventricular arrhythmias were studied in dogs with normal cardiac conduction systems and in dogs with surgically induced complete heart block. Glucagon, 20 μg/kg, effected conversion to a sinus rhythm in eight of nine animals with normal conduction systems, and in each instance the conversion occurred with a sinus tachycardia whose rate exceeded the rate of pre-existing ventricular arrhythmia. The one animal which failed to convert to a sinus rythm did not develop a sinus nodal rate faster than the rate of the ventricular arrhythmia. In 10 animals with ouabain-induced ventricular arrhythmias atrial pacing was employed to overdrive the arrhythmia, and in 6 cases this was successful. In all 6 experiments subsequent administration of glucagon after pacing resulted in conversion to a sinus rhythm at a rate greater than the minimum atrial pacing rate required to effect capture of the ventricules. In 4 of the 10 animals neither atrial overdrive nor glucagon were successful in effecting sinus conversion, but ventricular rate was slowed by lidocaine. In addition, in 5 animals with complete heart block and ouabain-induced ventricular tachycardia which were given glucagon, 20 μg/kg, there was no change in the tachycardia and no change in the ECG pattern associated with the arrhythmia. It was concluded that the antiarrhytmic action of glucagon in this arrhythmia is mediated through a supraventricular action to elevate sinus rate above that of the dominant ventricular focus and thus allow a return to dominance of the sinus node.