鼠脑血管痉挛时尼莫地平对体感诱发电位的影响

目的 探讨蛛网膜下腔出血（SAH）后脑血管痉挛（CVS）对体感诱发电位（SEP）的影响，及尼莫地平（ND）的保护作用。方法 对单纯SAH组和ND处理组大鼠观察手术前后基底动脉管径，并检测24h内局部脑血流量（rCBF)、SEP潜伏期及脑组织内皮素-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含量显著增加，ND处理组大鼠上述变化均较轻。结论 SAH后CVS可通过脑血流的降低，脑组织ET-1增加而导致SEP潜伏期延长，ND通过拮抗脑组织ET-1变化而对之具有保护作用。

Effect of nimodipine onsomatosensory evoked potential in rats with cerebral vasospasm following subarachnoidhemorrhage

Objective　 To investigate the effect of cerebral vasospasm(CVS) on somatosensory evoked potential (SEP) following subarachnoid hemorrhage，and the protective effect of nimodipine. Methods　Rats were divided into pure SAH group and ND-treated group. Diameter of basilar artery before and 0.5h after operation was measured, and dynamic changes of regional cerebral blood flow (rCBF), Latency of SEP , as well as endothelin-1 level in brain tissue within 24h were determined. Results　In SAH group, diameter of basilar artery was decreased markedly. rCBF was reduced significantly immediately after SAH, retaining in 24h. Latency of SEP was delayed from 1h to 24h, and endothelin-1 in brain tissue was increased simultaneously. Nimodipine significantly antagonized above pathological alterations. Conclusion　CVS after subarachnoid hemorrhage leads to delay of SEP latency via the decrease of cerebral blood flow and increase of endothelin-1 in brain tissue , which may be antagonized by nimodipine.