Cerebral arteries have an abundant supply of adrenergic nerve fibers which are believed to release vasoactive substances responsible for the induction of cerebral vasospasm. To assess the importance of adrenergic nerves in this phenomenon, high doses (600 μg/ml) of 6-hydroxydopamine (6-OHDA) were used to produce in vitro chemical sympathectomy in bovine middle cerebral artery. 6-OHDA reduced catecholamine fluorescence to undectable limits. H3-norepinephrine re-uptake was reduced to 1.5% of intact controls. Arterial norepinephrine content was reduced by 92%.
Contractile responses to norepinephrine, serotonin, and fresh human whole blood were modestly reduced after denervation. This reduction was probably due to alpha receptor inactivation by 6-OHDA, because after protection of the alpha receptors with phentolamine the vessel response was the same as in untreated controls. Contractions in response to aged human whole blood were not affected by denervation. The results suggest that the endogenous release of catecholamines does not play a major role in the initiation or spread of bloodinduced vasospasm in large cerebral arteries.