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

脑血管痉挛是蛛网膜下腔出血后的主要并发症之一，其发病机制尚不清楚。脑循环受EDRF（即NO）、内皮素等血管活性物质释放的血管活性物质以及血管周围神经纤维的CGRP、VIP、SP、NO等神经递质的调节。用自体动脉血注入枕大池造成大鼠和狗实验性蛛网膜下腔出血，大鼠第1天和狗第3天基底动脉出现严重的血管痉挛。蛛网膜下腔出血后，主要脑动脉内皮和外膜神经纤维中NO合酶的免疫阳性物质减少，并且NO介导的内皮依赖性血管舒张和NO介导的神经源性血管舒张在蛛网膜下腔出血后受损。提示NO介导的血管舒张机制受损可能参与了蛛网膜下腔出血后脑血管痉挛的发病机制。

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.