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.
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.
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.
方法采用线栓法制备大脑中动脉缺血再灌流模型。
Methods The focal cerebral ischemia and reperfusion model was made by thread embolism of MCA.
方法采用线栓法制备大脑中动脉缺血再灌流模型。
Methods We made the local cerebral ischemic reperfusion model with thread embolism of MCA.
方法建立家兔急性全脑缺血及缺血再灌流动物模型。
Methods The complete cerebral ischemia and ischemia-reperfusion model was made.
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.
减轻乃至防止无再灌流现象的发生对临床治疗有重要意义。
It is important to decrease and even prevent the phenomenon during clinical treatment of AMI.
目的：观察鼠全脑缺血再灌流后海马区NOS活性的变化。
Objective: To investigate the changes of the activity of nitric oxide synthase (NOS) in hippocampus during cerebral ischemia and reperfusion in rats.
目的：观察大鼠脑缺血再灌流时，脑组织病理改变的特点和时程。
Objectives: To observe the characteristics of neuronal change following cerebral ischemia and reperfusion.
目的探讨不同剂量巴曲酶对大鼠局灶脑缺血再灌流的保护作用。
Objective To study the protective effect of different dosage Batroxobin after cerebral ischemic reperfusion.
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.
目的探讨短暂脑缺血再灌流后突触传递功能的改变和神经系统的可塑性。
Objective To investigate the synaptic transmission function and neural plasticity after transient ischemia followed by repufusion.
用凝胶电泳及原位末端标记研究大鼠脑缺血再灌流后神经元的凋亡与坏死。
This article reports the apoptosis and necrosis of neurons following ischemia reperfusion in the brain of rats.
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.
再灌流0 .5小时组，缺血区皮质神经元GDNF弱阳性，缺血周边区中等阳性；
At 0.5 h of reperfusion, neurons in ischemic cortex showed GDNF weak positive, neurons in peri-ischemic regions showed GDNF moderate positive.
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).
在急性脑缺血与再灌流动物模型中采用硝酸镧块染法对神经细胞膜的通透性改变示踪。
Lanthanum nitrate block impregnation technic was used to demonstrate the neurocyte membrane permeability in the animal model of acute cerebral ischemia and reperfusion.
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.
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.
方法采用线栓法制作大鼠局灶性脑缺血再灌流模型，大脑中动脉阻塞2小时，再灌流4小时后观察梗死体积的变化。
Methods We made infarct models of rats with thread embolism and observed the changes of the infarct volume in rats which had re perfused 4 hours after 2 hours embolism.
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.
方法在一般性抢救治疗的基础上，再应用血液透析（HD）、血液灌流（HP）、血浆置换（PE）等血液净化技术抢救治疗急性药物中毒患者186例。
Methods 186 cases of acute drug poisoning received emergency treatment with the help of blood purification techniques such as HD, HP and PE.
方法在一般性抢救治疗的基础上，再应用血液透析（HD）、血液灌流（HP）、血浆置换（PE）等血液净化技术抢救治疗急性药物中毒患者186例。
Methods 186 cases of acute drug poisoning received emergency treatment with the help of blood purification techniques such as HD, HP and PE.
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