On the mechanism for bradycardia induced by acute systemic anoxia in the dog.

Abstract

The effects of acute systemic anoxia on heart rate were investigated in 46 anaesthetized, artificially ventilated and spontaneously breathing dogs. Severe anoxia produced by inhalation of 100 per cent nitrogen over a period of 1 to 3 min elicited in both groups of animals a biphasic response consisting of a primary tachycardia and secondary bradycardia. Whereas primary tachycardia was usually moderate, secondary bradycardia was very pronounced and amounted to a 45.8 per cent reduction of heart rate in artificially ventilated dogs, and to 67.2 per cent in dogs breathing spontaneously. Bilateral cervical vagotomy, atropinization and ganglionic blockade caused consistently a considerable reduction or abolition of anoxic bracycardia. On the contrary, elimination of the sympatho-adrenal system by means of spinal cord destruction and bilateral adrenalectomy was conducive to an evident enhancement of bradycardia. The intensity of bradycardia was not reduced following denervation of carotid and aortic baro- and chemoreceptors. On the contrary, denervation invariably resulted in a considerable increase of bradycardia. It is concluded that secondary anoxic bradycardia is mainly due to the increased tone of the vagal cardioinhibitory center, the local depressant action of anoxia on the heart itself being of minor importance. Increased vagal tone is opposed by the concomitant stimulation of the sympatho-adrenal system. Anoxic bradycardia cannot be regarded as resulting from stimulation of carotid and aortic receptors. It is, therefore, inferred that some other mechanism, reflex or central, is activated during acute systemic anoxia giving rise to the increased vagal discharge to the heart.