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NO被认为是一种自由基,与脑缺血关系密切,可能对缺血性脑损伤有直接的影响。方法:本文在建立线栓法制成大脑中动脉缺血模型的基础上,测定缺血侧与非缺血侧脑组织NO,SOD,LPO等含量的变化。结果:缺血早期,缺血侧与非缺血侧脑组织NO增加的速度很快,推测与NOS活性增加有关,也可能是脑缺血后产生神经毒性的早期反应;缺血侧脑组织SOD显著下降,LPO上升,表明由于自由基生成过多,SOD消耗过多,清除自由基的能力下降,这些早期的神经毒性作用在缺血性脑血管病的发病机制方面的意义值得深入研究。结论:缺血组织产生大量LPO及NOS活性增加,NO合成增多,自由基的堆积可能是脑组织损伤加重的重要因素。
NO is considered as a free radical, and is closely related to cerebral ischemia, which may have a direct impact on ischemic brain injury. Methods: Based on the establishment of a middle cerebral artery occlusion (MCAO) model by thread plug method, the content of NO, SOD and LPO in the ischemic and nonischemic brain tissues were determined. Results: In the early stage of ischemia, NO increased rapidly in the ischemic and nonischemic brain, suggesting that the increase of NOS activity may be an early response to neurotoxicity after cerebral ischemia. The expression of SOD And LPO increased, indicating that the role of these early neurotoxicity in the pathogenesis of ischemic cerebrovascular disease deserves further study because of excessive free radical production, excessive SOD consumption and decreased ability to scavenge free radicals. CONCLUSION: A large number of LPO and NOS activity increase, NO synthesis increases and accumulation of free radicals in ischemic tissue may be an important factor of brain injury.