方法采用家兔全脑缺血再灌流损伤模型。
Methods The rabbit model of acute complete cerebral ischemia and reperfusion were used.
方法：建立整体动物心肌缺血-再灌流损伤模型。
METHODS: The ischemia-reperfusion model were developed in rat heart in vivo.
本实验提示巴曲酶对脑缺血再灌流损伤所引起的细胞凋亡有抑制作用。
The present study strongly indicate that batroxobin inhibits apoptosis induced by cerebral ischemia reperfusion injury.
方法建立家兔心肌缺血再灌流损伤模型，通过原位杂交技术观察研究。
Methods A rabbit model of myocardial ischemia and reperfusion injury was established, and HSP70mRNA in myocardium was detected by in situ hybridization histochemistry.
自由基介导的脂质过氧化反应在脊髓缺血及缺血后再灌流损伤中具有重要作用。
The effects of lipid peroxidation initiated by free radicals contributed seriously to spinal cord ischemia and postischemic reperfusion injury.
方法建立大鼠急性脑缺血再灌流损伤模型，用原子分光光度仪检测脑组织电解质含量。
Methods Cerebral ischemia reperfusion injury model was produced in rats. The electrolyte contents were measured with atomic absorption spectrophotometer(AAS).
结论：手术组DNA和RNA荧光反射不清，可能与脑缺血再灌流损伤中氧化应激引起DNA链断裂有关。
CONCLUSION: the illegibility of DNA and RNA fluorescent response in operation group is related with the breakage of DNA chain induced by oxidative stress during cerebral ischemia-reperfusion injury.
提示氧自由基可能损害细胞色素氧化酶活性，细胞色素氧化酶活性降低在肾缺血再灌流损伤中可能起重要作用。
These results suggest that oxygen free radicals may damage the activity of cytochrome oxidase, the reduction of which may play an important role in the injury of renal ischemia and reperfusion.
目的观察多聚ADP 核糖聚合酶（PARP）在脑缺血再灌流损伤中的表达，探讨PARP在细胞凋亡中的作用。
Objective: To observe the expression of poly (ADP-ribose) polymerase (PARP) in focal cerebral ischemia with reperfusion injury and explore the role of PARP in apoptosis.
环氧化酶- 2 (COX - 2)及其代谢产物可通过对脉管系统、血脑屏障和神经元本身的损伤，参与脑缺血再灌流后损伤的机制。
Cyclooxygenase-2 (COX-2) and its metabolic products can be involved in the mechanism of the ischemic brain injury through destructing the vascular system, blood-brain barrier and the neuron.
结论再灌流前应用山茛菪碱能减少再灌流后氧自由基的产生，可减轻缺血—再灌流对移植肝脏的损伤。
Conclusions the use of anisodamine before reperfusion could reduce the production of oxygen derived free radical, therefore alleviate the injury of grafted liver caused by ischemia reperfusion.
结果表明较长时间缺血后再灌流加重组织损伤。
The results demonstrate that reperfusion after prolonged ischemia exaggerates tissue injury.
结论内皮素受休拮抗剂BQ- 123对全脑缺血再灌流引起海马区神经元损伤有部分保护作用。
Conclusion BQ-123 is useful in preventing the neuronal damage following the cerebral ischemia reperfusion in rats.
目的探讨肠缺血再灌流引起肺损伤的细胞机制。
Objective To investigate the relationship bet we en lung injury from intestinal ischemia-reperfusion and polymorphonuclear neutrophils in rats.
结论：SND有抗大鼠肺缺血-再灌注损伤作用，其机制可能与清除氧自由基和改善组织灌流有关。
CONCLUSION: These results indicate that SND may have a protective effect on ischemia-reperfusion injured lung by its antioxidant activity and by adjusting NO level.
结论：SND有抗大鼠肺缺血-再灌注损伤作用，其机制可能与清除氧自由基和改善组织灌流有关。
CONCLUSION: These results indicate that SND may have a protective effect on ischemia-reperfusion injured lung by its antioxidant activity and by adjusting NO level.
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