Inhalation of hypoxic gas (4% O2) for 15 seconds inhibited baroreflex vagal bradycardia via a direct central action in anaesthetized rats.
It is known that arterial baroreflexes are suppressed in stressful conditions. The present study was designed to determine whether and how hypoxia affects arterial baroreflexes, especially the heart rate component, baroreflex vagal bradycardia. In chloralose-urethane-anaesthetized rats, baroreflex vagal bradycardia was evoked by electrical stimulation of the aortic depressor nerve, and the effect of 15 s inhalation of hypoxic gas (4% O2) was studied. Inhalation of hypoxic gas was found to inhibit baroreflex vagal bradycardia. The inhibition persisted after bilateral transection of the carotid sinus nerve. Cervical vagus nerves were cut bilaterally and their peripheral cut ends were stimulated to provoke vagal bradycardia of peripheral origin so as to determine whether hypoxia could inhibit vagal bradycardia by acting on a peripheral site. In contrast to baroreflex vagal bradycardia, the vagus-induced bradycardia was not affected by hypoxic gas inhalation. It is concluded that baroreflex vagal bradycardia is inhibited by hypoxia and the inhibition is largely mediated by its direct central action.
Kongo et al. (Fri,) reported a other. Hypoxic gas (4% O2) inhalation was evaluated on Baroreflex vagal bradycardia. Inhalation of hypoxic gas (4% O2) for 15 seconds inhibited baroreflex vagal bradycardia via a direct central action in anaesthetized rats.