Cholinergic Factor in Auricular Fibrillation

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Abstract
Acetyl-beta-methyl choline (Mecholyl) applied to the surface of the exposed auricle predisposes the auricle to the development of auricular fibrillation, particularly when it is potentiated by an anti-esterase (Prostigmine). The essential feature of initiation of arrhythmia is repetition of impulses at a rapid rate reaching as high as 3000/minute, when recorded from local electrodes on the surface of the auricles. Gradations in tendency toward repetition exist. In the most active preparations repetition will follow a single spontaneous or induced impulse without regard to its position with relation to other beats. In less active preparations repetition is induced by the close coupling of 2 impulses. The degree of repetitiveness is increased by increased cholinergic activity. Cholinergic treatment shortens auricular refractory period, curtails monophasic action current, and produces low-voltage, nonpropagated oscillations of the after-wave at a rate comparable to fibrillation. It is suggested that oscillations may increase in voltage to threshold intensity and serve as pacemaker potentials, producing local discharges at high frequencies. Other evidence suggests that both at onset and termination of fibrillation this kind of pacemaking activity is involved rather than reentrant excitation via circus motion. Direct records of auricular fibrillation exhibit spindling similar to that seen in discharges from the brain. It was assumed that their appearance in the brain depends upon circus motion. This possibility as far as the heart is concerned was discussed.

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