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目的 :探讨诱导型一氧化氮合酶 (inducednitricoxidesynthase ,iNOS)、神经型一氧化氮合酶 (neuronalni tricoxidesynthase ,nNOS)对老年大鼠不完全性脑缺血小脑的影响。方法 :建立老年大鼠不完全性脑缺血动物模型 ,应用免疫组织化学染色方法检测iNOS ,nNOS在小脑的表达 ,用透射电镜观察小脑的超微结构变化。结果 :缺血30min后再灌注 6 ,12 ,2 4,48h组浦肯野细胞nNOS活性显著升高 (P <0 0 0 1) ,假手术组、缺血 30min立刻取材、缺血 30min后再灌注 1h和 96h组nNOS微量表达 ;而iNOS在小脑皮质不表达 ,髓质中有少量神经细胞中度表达。电镜下 48h和 96h组浦肯野细胞损伤较重。结论 :由nNOS诱导的一氧化氮 (nitricoxide ,NO)是脑缺血后神经元迟发性损伤的重要因素之一
Objective: To investigate the effects of inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS) on incomplete cerebral ischemia in aged rats. Methods: The animal model of incomplete cerebral ischemia in aged rats was established. The expression of iNOS and nNOS in cerebellum was detected by immunohistochemical staining. The ultrastructure of cerebellum was observed with transmission electron microscope. RESULTS: The nNOS activity of Purkinje cells increased significantly at 6, 12, 2, and 48 hours after reperfusion at 30 min after ischemia (P <0.01). In the sham operation group, the animals were sacrificed 30 min after ischemia and 30 min after ischemia However, iNOS was not expressed in the cerebellum and there was a small amount of nNOS in the medulla. 48h and 96h under electron microscopy Purkinje cell injury heavier. Conclusion: Nitric oxide (NO) induced by nNOS is one of the important factors of delayed neuronal injury after cerebral ischemia