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作 者:刘友尧[1] 张洪[2] 许国英[2] 吴秀丽[2] 慕容慎行[2]
机构地区:[1]福建医科大学生物化学教研室,福州350004 [2]福建医科大学附属第一医院神经内科,福建省神经病学研究所福州350005
出 处:《福建医科大学学报》2000年第1期36-38,共3页Journal of Fujian Medical University
摘 要:目的 研究大鼠脑缺血再灌流后大脑皮层、海马、纹状体和小脑组织一氧化氮合酶 (NOS)的变化。 方法 采用放射免疫法检测脑组织中 NOS的活性。 结果 大鼠脑缺血后 5 min,各脑区结构型 NOS(c NOS)活性明显升高 ,持续到脑缺血 30 m in,脑缺血 30~ 6 0 min开始下降 ;诱导型 NOS(i NOS)活性在脑缺血后 10~ 15 m in开始升高 ,并持续到脑缺血 6 0 min;脑缺血 30 min再灌流 15 min,各脑区 c NOS和 i NOS活性明显高于缺血 30 m in(P<0 .0 5或 P<0 .0 1)。 结论 提示脑缺血再灌流时脑组织 NOS活性增强 ,采用特异 NOS抑制剂可能有助于阻断脑缺血再灌流时由一氧化氮 (NO)介导的脑损伤作用。Objective\ To study the change of nitric oxide synthase(NOS) in rat cerebral cortex,hippocampus,striatum and cerebellum during cerebral ischemia/reperfusion.\ Methods\ The activity of constitutive NOS(cNOS) and inducible NOS(iNOS) were measured with radioimmunoassay.\ Results\ The activity of cNOS in four regions significantly increased at 5 min,and decreased in cerebral cortex,hippocampus and striatum at 60 min,in cerebellum at 15 min.\ The activity of iNOS markerly increased in cerebral cortex and striatum at 15 min,in hippocampus and cerebellum at 10 min,and persisted to 60 min.\ After 30 min ischemia plus 15 min reperfusion,the activity of cNOS and iNOS in four regions significantly increased compared with 30 min ischemia(P<0 05 or P<0 01).\ Conclusion\ The activity of cNOS and iNOS were significantly higher in rat during cerebral ischemia/reperfusion.\ Using specific NOS inhibitors to suppress the activity of NOS may assist in the treatment for cerebral ischemia.\;
分 类 号:R741.02[医药卫生—神经病学与精神病学]
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