Effect of subarachnoid hemorrhage on contractile responses and noradrenaline release evoked in cat cerebral arteries by histamine.

This study analyzes the changes induced by subarachnoid hemorrhage (SAH) on the contractile responses and the noradrenaline release evoked in cat cerebral arteries by histamine. The dose-dependent vasoconstriction induced by histamine on the cerebral arteries of normal cats was significantly reduced by diphenhydramine and phentolamine. When SAH was produced 3 and 7 days before the experiment, the histamine-induced vasoconstriction also decreased. Thereafter, a tendency to normalization in the contractile vascular responses was observed such that in 15 days after the hemorrhage it was not significantly different from that found in controls animals. The decrease in the contractile responses to histamine provoked by SAH was similar to that seen after pretreatment with intracisternal injections of 6-hydroxydopamine. The amount of radioactivity released by histamine following preincubation with 3H-noradrenaline from the cerebral arteries of cats exposed to SAH 3, 7, and 15 days before the experiment was significantly reduced when compared with controls. Moreover, the basal level of tritium release and the radioactivity retained at the end of the experiment were also decreased after SAH. These decreases were less marked 15 days after SAH. Intracisternal injections of 6-hydroxydopamine 3, 7, and 15 days prior to the assay, and the removal of both superior cervical ganglia 15 days before the experiment, also markedly reduced these three parameters. These results indicate that histamine releases noradrenaline from cat cerebral arteries, and SAH produces a transient denervation of the perivascular adrenergic nerve endings. The inhibition of the histamine-induced vasoconstriction observed after SAH might be explained by the impairment of the indirect adrenergic mechanism involved in the overall contractile response elicited by this amine in cerebral arteries. According to the present findings, histamine does not seem to play a significant role in the production of the cerebral vasospasm occurring after SAH.