Relationship between Endothelin-1 and Ischemic Brain Damage after Subarachnoid He morrhage and Protective Effect of Ginkgo Biloba Extract

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) on it. Methods: Noncraniotomy SAH models of Wistar rat were divided into SAH group and GBE treated group, the diameter of basilar artery (BA), 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 steadily in 24 hours after SAH. Spasm of BA occurred half an hour after SAH and neurons of hippocampus CA1 region were 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.

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

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。

一氧化氮与蛛网膜下腔出血后缺血性脑损害关系和银杏叶制剂的保护作用

目的探讨一氧化氮（ＮＯ）与蛛网膜下腔出血（ＳＡＨ）后缺血性脑损害的关系和银杏叶制剂（ＧＢＥ）的保护作用。方法应用非开颅大鼠模型，对ＳＡＨ组和ＧＢＥ组测量基底动脉（ＢＡ）管径并观察２４ｈ内微区脑血流量（ＣＢＦ）和颅内血清ＮＯ水平动态改变，３ｄ后对海马ＣＡ１区行病理检查。结果ＳＡＨ后ＣＢＦ和血清ＮＯ降低，ＢＡ痉挛，海马ＣＡ１区神经元明显受损。ＧＢＥ使上述改变减轻。结论ＳＡＨ时血清ＮＯ减少是导致缺血性脑损害的重要因素。

大鼠脑血管痉挛时血及脑组织NO、内皮素改变和银杏叶制剂的作用

目的 探讨 Ｎ Ｏ、内皮素（ Ｅ Ｔ） 与蛛网膜下腔出血（ Ｓ Ａ Ｈ） 后脑血管痉挛（ Ｃ Ｖ Ｓ） 的关系和银杏叶制剂（ Ｇ Ｂ Ｅ） 的防治作用。方法 对假手术组、单纯 Ｓ Ａ Ｈ 模型组和 Ｇ Ｂ Ｅ 处理组大鼠检测２４ 小时内局部脑血流量、血及脑组织 Ｎ Ｏ、 Ｅ Ｔ 含量，并测基底动脉管径及行海马病理检查。结果 Ｓ Ａ Ｈ 造成局部脑血流量持续下降，并有基底动脉痉挛，海马 Ｃ Ａ１ 区神经元明显受损；血 Ｎ Ｏ 减少、 Ｅ Ｔ 增多，脑组织 Ｎ Ｏ、 Ｅ Ｔ 均增加； Ｇ Ｂ Ｅ 使上述改变均减轻。结论 血 Ｎ Ｏ 减少、 Ｅ Ｔ 增多促使 Ｓ Ａ Ｈ 后 Ｃ Ｖ Ｓ 发生，脑组织 Ｎ Ｏ 和 Ｅ Ｔ 增加加重脑损伤； Ｇ Ｂ Ｅ 通过逆转 Ｎ Ｏ、 Ｅ Ｔ 异常改变而发挥保护作用。