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目的 :探讨蛛网膜下腔出血 (SAH)后脑血流量、体感诱发电位 (SEP)潜伏期的改变及其与一氧化氮 (NO)的关系。方法 :对假手术对照组和SAH模型组大鼠检测 2 4h内局部脑血流量 (rCBF)、SEP潜伏期和血清及脑组织NO含量动态变化。结果 :非开颅刺破Willis环的方法可成功地诱发SAH。SAH后rCBF立即降低 ,在 2 4h内无恢复趋势。SEP潜伏期于SAH后 1h开始至 2 4h明显延长。血清和脑组织NO含量于SAH后 1h开始分别显著减少和明显增加 ,并持续 2 4h。结论 :SEP对SAH后脑缺血损伤的判断有重要意义。血清NO减少及脑组织NO增加分别在脑血管痉挛发生及加重脑缺血损伤中起重要作用
Objective: To investigate the changes of cerebral blood flow and somatosensory evoked potential (SEP) latency after subarachnoid hemorrhage (SAH) and its relationship with nitric oxide (NO). Methods: The sham operation control group and SAH model group rats were detected within 24 hours of local cerebral blood flow (rCBF), SEP latency and serum and brain tissue NO content dynamic changes. Results: Non-craniotomy punctured Willis rings successfully induced SAH. RCBF immediately after SAH decreased, no recovery trend within 24 hours. SEP latency in SAH after 1h to 24h significantly prolonged. NO content in serum and brain tissue significantly decreased and significantly increased from 1 hour after SAH, respectively, and continued for 24 hours. Conclusion: SEP is of great significance in judging cerebral ischemia injury after SAH. Reduced serum NO and increased NO in brain tissue play an important role in the development of cerebral vasospasm and in aggravating cerebral ischemic injury