脑血管痉挛后体感诱发电位潜伏期变化和尼莫地平的影响  

Changes of latency of somatosensory evoked potential and influence of nimodipine during cerebral vasospasm following subarachnoid hemorrhage

作　　者：孙保亮[1] 夏作理[1] 杨明峰[1] 邱平明[1] 陈连壁[2] 

机构地区：[1]泰山医学院附属医院神经内科,山东泰安271000 [2]山东医科大学生理教研室,山东济南250021

出　　处：《泰山医学院学报》2000年第3期179-181,共3页Journal of Taishan Medical College

摘　　要：目的　探讨尼莫地平对蛛网膜下腔出血 (SAH)后脑血管痉挛所致神经功能损伤的保护作用。方法　对单纯SAH组和尼莫地平处理组大鼠观察手术前后基底动脉管径 ,并检测局部脑血流量 (rCBF)、体感诱发电位(SEP)及脑组织内皮素 1(ET 1)含量的动态变化。结果　SAH组大鼠在诱导SAH后rCBF立即降低 ,并持续 2 4h ,同时有基底动脉痉挛 ;SAH后 1h开始至 2 4hSEP潜伏期逐渐延长 ,脑组织ET 1含量显著增加。尼莫地平使上述变化均明显减轻。结论　尼莫地平对SAH后脑血管痉挛所致神经功能损伤具有保护作用 ,其机理之一为拮抗脑组织ETObjective: To investigate the changes of latency of somatoevoked potential(SEP) and influence of nimodipine during cerebral vasospasm following subarachnoid hemorrhage(SAH). Methods: Rats were divided into pure SAH group and nimodpine treated group. Diameters of basilar artery before and 0.5 h after operation were measured, and dynamic changes of regional cerebral blood flow (rCBF), SEP, endothelin 1 levels in brain tissue within 24 h were determined. Results: In SAH group, diameter of basilar artery was decreased markedly. rCBF was reduced immediately after SAH and retained in 24 h. Latency of SEP was delayed from 1h to 24 h, and endothelin 1 in brain tissue was increased simultaneously. Nimodipine significantly antagonized pathological alterations of above parameters. Conclusion: Cerebral vasospasm after SAH leads to neurological deficit which may be alleviated by nimodipine via antagonizing the pathological alterations of endothelin 1 in brain tissue.

关 键 词：蛛网膜下腔出血 脑血管痉挛 体感诱发电位 

分 类 号：R743.35[医药卫生—神经病学与精神病学]