摘要
目的探讨蛛网膜下腔出血（ＳＡＨ）后继发性脑缺血损伤和尼莫地平（ＮＤ）的保护作用。方法利用大鼠ＳＡＨ模型，对单纯ＳＡＨ组和ＮＤ处理组检测术前及ＳＡＨ后２４ｈ内脑微区血流量（ＣＢＦ）、体感诱发电位（ＳＥＰ）和脑组织一氧化氮（ＮＯ）含量，并于ＳＡＨ后３ｄ对海马组织行病理检查。结果单纯ＳＡＨ组大鼠在产生ＳＡＨ后ＣＢＦ立即降低，并持续２４ｈ，ＳＥＰ潜伏期从ＳＡＨ后１ｈ开始逐渐延长，３ｄ后海马ＣＡ１区神经元明显损伤；脑组织ＮＯ含量在ＳＡＨ后１ｈ至２４ｈ显著增加。ＮＤ处理组的上述改变均较单纯ＳＡＨ组明显减轻。结论ＳＡＨ可导致继发性脑缺血损伤，其原因之一为脑组织ＮＯ大量增加；ＮＤ通过拮抗脑组织ＮＯ的病理变化而减轻ＳＡＨ后继发性脑缺血性损伤。
Objective To investigate the secondary ischemic cerebral damage following subarachnoid hemorrhage(SAN) and protective effects of nimodipine. Methods Rat SAH models were used and amimals were divided into pure SAH group and nimodipine treated group.Rats in both groups underwent measurement of dynamic changes of microregional cerebral blood flow (CBF), somatosensory evoked potential(SEP) and nitric oxide(NO) levels in brain tissues before and within 24h after induction of SAH.Pathological examination of hippocampus was carried out 3d later. Results In pure SAH group,CBF decreased immediately after SAH being produced,with no tendency to recover within 24h. The incubation periods of SEP delayed progessively from 1h to 24h. Neurons in CA1 region of hippocampus damaged severely.Brain NO levels increased from 1h to 24h after SAH. Nimodipine alleviated all of above pathological alterations. Conclusions SAH may give rise to secondary ischemic cerebral damage whose mechanisms may involve the increase of brain NO levels. Nimodipine exerts its protective effects by antagonizing the pathological accumulation of brain NO.
出处
《中国微循环》
1999年第2期79-81,共3页
Journal of Chinese Microcirculation
关键词
蛛网膜下腔出血
继发性缺血
脑缺血
尼莫地平
Subarachnoid hemorrhage Cerebral ischemia Somatosensory evoked potential Nitric oxide Nimodipine
