Bilateral lesions of the fastigial nucleus prevent the recovery of blood pressure following hypotension induced by hemorrhage or administration of endotoxin.

The present studies were undertaken to determine if bilateral lesions of the fastigial nuclei of the cerebellum would impair the recovery and maintenance of mean arterial blood pressure during hypotension caused by hemorrhage or administration of endotoxin. We had shown previously that cerebellectomy would produce such an impairment, and the fastigial nuclei were implicated as the specific area involved due to the known pressor response observed when they are stimulated electrically. Chloralose-anesthetized dogs were made hypotensive by administration of E. coli endotoxin or hemorrhage to 50 mm Hg and observed over the subsequent 3 h. Dogs with fastigial nucleus lesions had a significantly lower mean arterial pressure during both the recovery and maintenance phases when compared with intact animals under both hypotensive protocols. In the hemorrhage study, a significant number of lesioned animals died whereas none of the controls died. Lesion of the fastigial nuclei produced an impairment similar to that seen with cerebellectomy. It is concluded that the fastigial nuclei play an important role in the recovery of blood pressure following a hypotensive episode.

The effect of angiotensin and vasopressin blockade separately and in combination with cerebellectomy on recovery from hemorrhagic hypotention.

We demonstrated previously that cerebellectomy or ablation of the fastigial nuclei (FN) in the dog impairs markedly the restoration of blood pressure and increases the death rate after severe hypotension. Angiotensin (AII) and vasopressin (AVP) participate in the pressor response to hypotension, and plasma levels of both are increased by electrical stimulation of the FN. The present studies examined the importance of the FN in mediating the secretion of AII and AVP after hemorrhage to 50 mm Hg. Cerebellectomy reduced significantly both the rate of recovery and level of maintenance of blood pressure after hemorrhage. Blockade of conversion of AI of AII with captopril produced a similar deficit, and combination of both treatments produced a greater impairment than either alone. Treatment with an AVP antagonist decreased the level of maintenance of blood pressure but not be initial rate of recovery. The AVP antagonist in combination with cerebellectomy did not produce a greater deficit than cerebellectomy alone. This would suggest that although the cerebellum mediates some activation of the renin-angiotensin system during severe hypotension, it may mediate most of the AVP secretion under these conditions.