The ability of the carotid baroreflex to produce cardiac slowing during arterial hypoxia was investigated in dogs anesthetized with morphine-chloralose. The heart rate response to baroreflex stimulation decreased by about 20% at an arterial O2 tension (PaO2) of 65-70 Torr and by over 60% at a PaO2 of 15-20 Torr. After the aortic nerves were cut bilaterally, baroreflex stimulation produced greater cardiac slowing (P less than 0.001) during arterial hypoxia (PaO2 20 Torr) than at the same PaO2 with intact aortic nerves. The systemic depressor response to baroreflex stimulation was reduced in a qualitatively similar manner but with greater variability. After atropine (0.2 mg/kg iv) or vagal transection the heart rate response to baroreflex stimulation during hypoxia was not suppressed from its control. Perfusion of the head with hypoxic blood in carotid-denervated animals also reduced the baroreflex bradycardia. The results suggest that the vagal component of the baroreflex bradycardia is suppressed during arterial hypoxia both by a reflex mediated by the aortic chemoreceptors and by a direct effect of hypoxia on the central nervous system.
Effects of Unilateral and Bilateral Carotid Baroreflex Stimulation on Cardiac and Neural Sympathetic Discharge Oscillatory Patterns