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背景:一氧化氮在神经系统中的作用是近10年来的研究热点之一,而其在脑缺血过程中对神经细胞的损伤的何保护性作用?目的:研究一氧化氮在局灶性脑缺血再灌流过程中对病理改变的影响,并探讨其机制。设计:完全随机对照开放实验。地点和对象:实验地点:吉林大学第一医院神经科研究室;研究对象:Wistar大鼠70只,雌雄各半,体质量200～250g,由本校实验动物部提供。干预:利用N-硝基-左旋-精氨酸(N-nitro-L-arginine,NNLA)干预局灶性大鼠脑缺血模型。主要观察指标:通过光、电镜及未端脱氧核糖核酸介导生物素化脱氧尿嘧啶缺口未端标记(terminaldeoxyribonucleotidetransferase-mediateddUTP-biotinnickend-labeling,TUNEL)法观察局灶脑缺血大鼠脑组织的病理学改变。结果:缺血再灌1d时光镜下皮质、海马区均可见神经细胞呈坏死样改变;电镜下半影区神经细胞的改变仅见于核染色质凝集(类似凋亡小体)和小胶质细胞核变形,以细胞凋亡为主;小剂量给予NNLA干预后坏死和凋亡的病理改变均较手术对照组轻(P<0.01)。TUNEL显示与病理改变结果一致(P<0.01)。结论:局灶性脑缺血后,调节一氧化氮生成量在适当范围,可以保护、防止神经细胞进一步损伤。
BACKGROUND: The role of nitric oxide in the nervous system is one of the hot topics in recent 10 years. What protective effect does it have on neuronal damage during cerebral ischemia? OBJECTIVE: To study the role of nitric oxide in focal The influence of cerebral ischemia and reperfusion on pathological changes, and explore its mechanism. Design: Complete randomized controlled open experiment. Location and Subjects: Experimental Location: Department of Neurology, First Hospital of Jilin University; Study Object: Wistar rats 70, male and female, body weight 200 ~ 250g, provided by the Department of Laboratory Animal. Intervention: The focal cerebral ischemia model was induced by N-nitro-L-arginine (NNLA). MAIN OUTCOME MEASURES: The brain tissues of focal cerebral ischemia rats were observed by light, electron microscopy and terminal deoxyribonucleotide transferase mediated mediated urine (TUNA) -dependent labeling (TUNEL) Neo-Confucianism changes. Results: The neurons showed necrotic changes in the cortex and hippocampus at 1 day after ischemia-reperfusion. The changes of the neurons in the penumbra under electron microscope were found only in the chromatin condensation (similar apoptotic bodies) and microglial nuclei The morphological changes were mainly apoptosis. The pathological changes of necrosis and apoptosis after small dose administration of NNLA were lighter than that of the control group (P <0.01). TUNEL showed consistent with pathological changes (P <0.01). CONCLUSION: After focal cerebral ischemia, the production of nitric oxide can be regulated in a proper range, which can protect and prevent the further damage of nerve cells.