Cardiovascular Responses to Hypoxic Stimulation of the Carotid Bodies

The hemodynamic responses to hypoxic stimulation of the carotid bodies were investigated in the dog with controlled respiration. A dual, rotating disc oxygenator system was utilized to perfuse the vascularly isolated carotid region alternately with blood of high or low pO2. Perfusion of the carotid bodies with hypoxic blood caused a large reduction of heart rate. The bradycardia response was reduced, but not abolished, by vagotomy. However, the subsequent administration of hexamethonium completely abolished the response. The contractility of the atrium was reduced by carotid body hypoxia, and varying degrees of heart block were frequently observed. These responses were abolished by vagotomy and considered to be due to efferent vagal activity. Ventricular function curves showed that carotid body hypoxia usually caused a reduction, never an increase, of ventricular contractility. This indicates a reduction of sympathetic discharge to the heart. The reduction in heart rate after vagotomy and the reduction in ventricular contractility were associated with a concomitant increase of total peripheral resistance. These findings indicate that hypoxic stimulation of the carotid bodies causes a dichotomous sympathetic response, that is, a reduction of sympathetic discharge to the heart and a simultaneous increase of sympathetic discharge to the peripheral vasculature. Systemic hypoxia caused an increase of both ventricular contractility and total peripheral resistance. Consequently, the hemodynamic responses to systemic hypoxia cannot be entirely ascribed to a primary chemoreceptor reflex from the carotid bodies. It is suggested that the cardiac sympathetic responses seen in systemic hypoxia are due, at least in part, to direct hypoxic stimulation of the central nervous system.