蛛网膜下腔出血大鼠体感诱发电位和一氧化氮rn含量变化及银杏叶制剂的影响

摘要

目的：探讨蛛网膜下腔出血(SAH)后体感诱发电位(SEP)、血清及脑组织一氧化氮(NO)含量变化和银杏叶制剂(GBE)的影响。方法： 对假手术对照组，模型组和GBE处理组大鼠检测24 h内局部脑血流量(rCBF)、SEP和血清及脑组织NO含量动态变化。结果： SAH后rCBF立即降低，在24 h内无恢复趋势。SEP潜伏期于SAH后1 h开始明显延长。血清和脑组织NO含量于SAH后1 h开始分别显著减少和明显增加，并持续24 h。GBE有效阻止上述病理性改变。结论： SEP对SAH后脑缺血损害的判断有重要意义。血清NO减少、脑组织NO增加分别在脑血管痉挛发生及加重脑缺血损害中起重要作用。GBE通过逆转SAH后NO异常变化而减轻脑血管痉挛及其脑缺血性损伤。%AIM: To investigate the changes of somatosensory evoked potential(SEP), nitric oxide (NO) levels both in serum and in brain tissue after subarachnoid hemorrhage(SAH) and the influence of Ginkgo biloba extract(GBE) on them. METHODS: Wistar rats were divided into sham-operated group, pure SAH group and GBE-treated group. Dynamic changes of regional cerebral blood flow( rCBF),SEP, and NO levels both in serum and in brain tissue were detected within 24 hours after operation. RESULTS: In pure SAH group, rCBF decreased immediately after operation, with no tendency to recover within 24 hours. Latency of SEP delayed progressively from 1 hour to 24 hours after SAH.NO levels in serum and in brain tissue decreased and increased respectively from 1 hour to 24 hours after SAH. GBE effectively antagonized the changes of above parameters. CONCLUSION: SEP is useful in the judgement of cerebral ischemic damage after SAH. Decrease of serum NO and increase of brain NO are important factors leading to cerebral vasospasm and neural damage respectively after SAH. GBE relieves cerebral ischemic damage by reversing the pathological alterations of NO.