Abstract
Atrial fibrillation has been produced in isolated rabbit auricles suspended in medium of low K by stimulating (600–1200 /min.) in the presence of acetylcholine (3.0 x 10–4 gm/ml). The effects of acetylcholine, quinidine and stimulus frequency on the rate of loss of K by the auricle were investigated in an attempt to see if changes in permeability occurred with the onset of fibrillation. The thesis is developed that fibrillation begins at a time in the myocardium when the rate of outward flux of K, and possibly the inward flux of Na, exceeds a certain critical value (8.0–10.0 mm/kg tissue/5 min.). It is suggested that when this critical flux is exceeded, ectopic pacemakers (single or multiple) appear in the myocardial membrane, the maintenance of which requires the presence of acetylcholine in sufficient concentrations.