Abstract

Neural integration during arterial hypoxia was studied in sham-operated, rhinencephalic, thalamic, high mesencephalic, and pontine rabbits, 3 hours after operation under halothane anesthesia. All preparations except the pontine recovered normal movement and posture 40 to 60 minutes after the operation, and effects on the resting circulation specifically ascribable to transection were small. Activation of diencephalic, and to a lesser extent of rhinencephalic, centers was necessary to produce the large increase in autonomic peripheral resistance effect and the autonomic slowing of heart rate characteristic of normal rabbits. In animals with only pontine and high mesencephalic centers, the autonomic peripheral resistance effect was smaller and there was an autonomic rise in heart rate. The neocortex and rhinencephalon exerted inhibitory influences related to the effects of hyperventilation. Suprabulbar respiratory mechanisms were also activated during hypoxia, with diencephalic mechanisms limiting the reflex response mediated by the pontine centers and the cortex exerting disinhibitory effects on the diencephalic centers. The cardiorespiratory response at different degrees of hypoxia probably depends on differences in relative magnitude of inputs from the arterial chemoreceptors, baroreceptors, and lung inflation receptors, producing different degrees of excitation and inhibition of the various suprabulbar and bulbar centers.

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