Involvement of L-arginine-nitric oxide pathway in cerebral vasospasm

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Although cerebral vasospasm is one of the major complications after subarachnoid hemorrhage, its pathogenesis remains to be elucidated. Cerebral circulation is regulated by vasoactive substances released from vasoactive substances such as EDRF (i.e.NO) , endothelin, and also by neurotransmitters from perivascular nerve fibers such as CGRP,VIP,SP,NO.We investigated in the present study the possible involvement of NO in the occurrence of cerebral vasospasm after subarachnoid hemorrhage. Experimental subarachnoid hemorrhage was produced in rats and dogs by injecting autologous arterial blood into the cistema magna.Severe vasospasm was obtained in basilar arteries on Day 1 in rats and Day 3 in dogs. Immunopositive materials for NO synthase in the endothelium and in the adventitial nerve fibers of major cerebral arteries were reduced after subarachnoid hemorrhage, and NO mediated endothelium dependent vasorelaxations and NO mediated neurogenic vasorelaxations were impaired after subarachnoid hemorrhage. These results indicated that the impairement of NO mediated vasorelaxation mechanisms might be involved in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage.