Mechanisms of tachycardia caused by atropine in conscious dogs

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Abstract
Atropine (0. 2 mg.Ag) was given intravenously to trained conscious dogs before and after thoracic sympathectomy, treatment with reserpine (0. I mg/kg daily for 5 days), and treatment with propranolol (1 mg/kg, singly or in combination. Cardiac acceleration resulted in all cases, with an average maximum of 220 beats/min accompanied by minor increases in cardiac output and in systemic blood pressure. Stimulation of the vagus nerve in the anesthetized, atropinized dog resulted in an increase in heart rate characterized by delay in onset and persistence after stimulation had ceased. The increase in rate persisted after beta-adrenergic blockade but was abolished by hexamethonium bromide. The administration of acetylcholine to isolated blood-perfused hearts resulted in an increase in contractility abolished by beta-adrenergic blockade. It is proposed that the tachycardia seen in the conscious dog after atropine use is not adrenergic in nature but results from a central stimulant action of atropine, impulses passing via the vagus nerves to some cardiac structure which pharmacologically behaves like a ganglion. The postganglionic mechanism is unknown.