Multielectrode mapping of stimulus propagation was used to investigate arrhythmias, developing in atrial preparations of frogs after vagal stimulation. Vagal stimulation produced attacks of tachycardia (one to several dozens extra-excitations) in 10 of 16 specimens. In such cases, mapping demonstrated re-entry of the excitation wave that appeared where the front of the next excitation wave from the sinus went along the border of temporarily-unexcitable area during the recovery of excitability in vagus-inhibited atrial areas. The emergence of re-entry was possible, because the excitation wave length (lambda), was shortened owing to reduced refraction and speed of conduction under vagal effect. After myocardial tissue got rid of vagal influence, lambda increased, after which re-entry was no longer possible, and arrhythmia discontinued.