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孙保亮,夏作理,郑澄碧,李汶霞,房玉珍.内皮素-1与脑血管痉挛缺血性脑损害的关系及银杏叶制剂的保护作用[J].,1998,(11):677-679
内皮素-1与脑血管痉挛缺血性脑损害的关系及银杏叶制剂的保护作用
Relationship between Endothelin-1 and Ischemic Brain Damage after Subarachnoid Hemorrhage and Protective Effect of Ginkgo Biloba Extract
  
DOI:
中文关键词:  蛛网膜下腔出血  脑血管痉挛  缺血性脑损害  内皮素  银杏叶制剂
英文关键词:subarachnoid hemorrhage  cerebral vasospasm  ischemic brain damage  endothelin  Ginkgo biloba extract
基金项目:山东省科学技术委员会资助课题!(No.96 115 )
Author NameAffiliation
孙保亮 Sun Baoliang, Xia Zuoli, Zheng Chengbi, et al Department of Neurology, Institute of Microcirculation, Affiliated Hospital, Taishan Medical College, Shandong (271000 
夏作理 Sun Baoliang, Xia Zuoli, Zheng Chengbi, et al Department of Neurology, Institute of Microcirculation, Affiliated Hospital, Taishan Medical College, Shandong (271000 
郑澄碧 Sun Baoliang, Xia Zuoli, Zheng Chengbi, et al Department of Neurology, Institute of Microcirculation, Affiliated Hospital, Taishan Medical College, Shandong (271000 
李汶霞 Sun Baoliang, Xia Zuoli, Zheng Chengbi, et al Department of Neurology, Institute of Microcirculation, Affiliated Hospital, Taishan Medical College, Shandong (271000 
房玉珍 Sun Baoliang, Xia Zuoli, Zheng Chengbi, et al Department of Neurology, Institute of Microcirculation, Affiliated Hospital, Taishan Medical College, Shandong (271000 
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中文摘要:
      目的 :探讨内皮素 1 (endothelin 1 ,ET 1 )与蛛网膜下腔出血 (subarachnoidhem orrhage,SAH)后缺血性脑损害的关系和银杏叶制剂 (ginkgobilobaextract,GBE)的防治作用。方法 :应用非开颅大鼠模型 ,对SAH组和GBE组测量基底动脉 (basilarartery ,BA)管径并观察2 4h内微区脑血流量 (regionalcerebralbloodflow ,rCBF)和颅内血浆ET 1水平动态改变 ,3天后对海马CA1区行病理检查。结果 :SAH后rCBF迅速而持续降低 ,血浆ET 1浓度显著增加 ,BA痉挛 ,海马CA1区神经元明显受损。GBE使上述改变均减轻。结论 :SAH时ET 1增加是导致缺血性脑损害的重要因素 ,GBE通过拮抗ET 1病理性增多而减轻缺血性脑损害。
英文摘要:
      Objective: To investigate the role of endothelin 1 (ET 1) in development of ischemic brain damage after subarachnoid hemorrhage (SAH), and the protective effect of Ginkgo biloba extract (GBE). Methods: Wistar rat noncraniotomy models of SAH were divided into SAH group and GBE treated group, the diameter of basilar artery (BA) and dynamic changes of regional cerebral blood flow (rCBF) and ET 1 content of intracranial plasma within 24 hours after SAH of both groups were determined. And pathological examination of CA1 region of hippocampus was performed 3 days later. Results: rCBF decreased and ET 1 content increased obviously and retained in 24 hours after SAH. Spasm of BA occurred half an hour after SAH and neurons of hippocampus CA1 region was damaged severely. GBE could antagonize the above mentioned pathological changes effectively. Conclusion: Increase of ET 1 is an important factor leading to ischemic brain damage after SAH. GBE exerts its protective effect by antagonizing pathological increase of ET 1.
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