Rôle of Adrenergic Factors in the Production and Perpetuation of Atrial Flutter in the Dog

The rôle of adrenergic factors in the production and perpetuation of atrial flutter has been studied in dogs under pentobarbitone sodium anaesthesia. The adrenergic influence was (a) increased by sympathetic stimulation or by intravenous injection of adrenaline and noradrenaline and (b) decreased by depletion of cardiac stores of catecholamines by previous treatment of the animals with reserpine. Sympathetic stimulation, as well as adrenaline and noradrenaline increased the atrial rate in aconitine‐induced and post‐stimulatory atrial flutter, and in some cases the flutter was converted into fibrillation. Atropine sulphate only partially blocked the increase in flutter rate, but atrial fibrillation never occurred after atropine administration. In some cases of aconitine‐induced atrial flutter, as the peak effect of adrenaline was passing off the atrial rate fell below that of sinus rhythm for a few seconds, and then gradually increased to the control level. No such response was seen after noradrenaline administration. When cardiac stores of catecholamines were depleted by previous treatment of the animals with reserpine, aconitine produced long‐lasting atrial fibrillation in all the experiments. Atropine injection converted atrial fibrillation into slow rate atrial flutter. In such animals, electrical stimulation produced transient atrial fibrillation, the rhythm returning to normal sinus rhythm, a few seconds to a few minutes after the stimulation ceased. It was not possible to induce stable atrial flutter despite repeated attempts, and even after the administration of atropine. The mechanism of these findings is discussed.