Noradrenergic Mediation of Experimental Cerebrovascular Spasm

Abstract

Catecholamine fluorescent techniques demonstrate an abundant noradrenergic periarterial nerve plexus in the adventitia of the major intracranial vessels. After repeated spasm of these vessels, a marked reduction to complete absence of catecholamine fluorescence is noted. Seemingly, an exhaustion of noradrenalin stores from the nerve terminals has taken place. This has suggested the possibility of noradrenergic mediation of cerebrovascular spasm. Pharmacological depletion of the noradrenalin stores of this plexus produces a dilated vessel, but blood-induced vasospasm is not prevented. Alpha adrenergic blockade at the receptor prevents the induction of vasospasm and dilates both normal and spastic vessels above normal caliber. These data suggest that cerebral vasospasm is produced by substances acting at the alpha adrenergic receptor of the vessel wall, and that blood contains a vasoconstrictor substance capable of acting at the receptor site.