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

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２４ｈ，同时有基底动脉痉挛；ＳＡＨ后１ｈ开始至２４ｈＳＥＰ潜伏期逐渐延长，脑组织ＥＴ－１含量显

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

Objective: 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.