Carotid chemoreceptors and vagi in hypoxic and cyanide-induced tachycardia in the dog

Abstract

We investigated the mechanisms underlying heart rate changes resulting from systemic hypoxia in anesthetized artificially ventilated dogs with low control heart rate (less than or equal to 93 beats/min). We observed that systemic hypoxia evoked tachycardia in intact dogs that was not significantly different from that evoked in dogs with beta-adrenergic blockade (BB). Also, tachycardia elicited in dogs with BB plus spinal section at C3 (BBSS) was significantly greater than in dogs with BBSS plus bilateral section of carotid sinus nerves. Furthermore, under various anesthetics, intracarotid injection of sodium cyanide induced a tachycardia response in dogs with low control heart rate (less than or equal to 97 beats/min) and a bradycardia response in dogs with high control heart rate (greater than or equal to 130 beats/min). These results suggest that 1) when the resting cardiac parasympathetic tone is high, systemic hypoxia evokes tachycardia which is mediated predominantly through efferent vagus nerves and 2) the stimulation of carotid chemoreceptors causes excitation of both cardioacceleratory and cardioinhibitory reflexes, the resultant response being dependent on the prevalent autonomic drive.