Abstract

The influence of the trigeminal nerve on the cerebral circulation was investigated in chronically denervated cats during and after reversible four-vessel occlusion for 10 minutes combined with controlled hypotension (50 mm Hg). Postocclusive hyperemia 30 minutes after reperfusion was attenuated by up to 48% in cortical gray matter of the anterior, middle, and posterior cerebral artery territories on the side of trigeminal ganglionectomy. Similar results were observed for denervation accomplished by direct surgical ablation and by the topical application of capsaicin to a cortical branch of the middle cerebral artery. Denervation did not alter basal cerebral blood flow or the duration of hyperemia, nor did it impair the cerebrovascular response to hypercapnia. These data demonstrate the importance of neurogenic mechanisms in the development of postischemic hyperperfusion and suggest that strategies directed at blocking axon reflex-like mechanisms may be beneficial in reducing the morbidity that follows severe cortical hyperemia.