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The contribution of the fastigial nucleus and the vestibular nerves (eighth cranial nerves) to the orthostatic reflexes in anesthetized, paralyzed cats was studied. Bilateral lesions of the rostral fastigial nucleus resulted in impairment of the reflex changes in blood pressure, femoral arterial flow, and resistance evoked by head-up tilting to 30° or 60°. The deficit consisted of an increase in the magnitude of the initial fall in blood pressure during tilting. The effects on blood pressure were paralleled by decreased vasoconstriction in the femoral artery. Extracranial lesions of the vestibular nerves produced comparable deficits which were not enhanced by subsequent lesions of the fastigial nucleus. Denervation of the baroreceptors impaired the reflexes, and subsequent lesion of the fastigial nucleus increased this deficit. The pressor response evoked by electrical stimulation of the rostral fastigial nucleus also reversed the deficit in orthostasis produced by hemorrhage. Small doses of sodium pentobarbital which did not alter the resting blood pressure or the pressor response to carotid occlusion impaired the responses to stimulation of the fastigial nucleus and tilting. Therefore, the rostral fastigial nucleus, which might be triggered by the vestibular apparatus, appears to participate in concert with the baroreceptors in the initiation and possibly the maintenance of the orthostatic reflexes.
Doba et al. (Tue,) studied this question.