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。

Relationship between nitric oxide, endothelin and cerebral vasospasm in rats with subarachnoid hemorrhage and effect of Ginkgo biloba extract

Objective To investigate the relationship between nitric oxide (NO),endothelin (ET) and cerebral vasospasm (CVS) following subarachnoid hemorrhage (SAH), and the protective effect of Ginkgo biloba extract (GBE). Methods The rats were divided into shamoperation group, simple SAH model group and GBE treated group. Regional cerebral blood flow (rCBF), NO and ET in both blood and brain tissue within 24 h after operation were detected. Diameter of basilar artery and morphologic changes of hippocampus were observed. Results SAH caused persistent reduction of rCBF within 24 h, and led to spasm of basilar artery. Neurons of hippocampus CA1 region were damaged severely 3 days after SAH. NO in blood was decreased while that in brain tissue increased. Both blood and brain ET levels were increased. GBE effectively antagonized above alterations. Conclusion Decrease of NO and increase of ET in blood are involved in the development of CVS following SAH, while increase of NO and ET in brain tissue contributes to brain damage due to ischemia. GBE exerts therapeutic effect by inhibiting the pathological changes of NO and ET.