缺氧预处理对缺血缺氧脑组织超微结构与自由基的影响

目的 观察缺氧预处理对缺血缺氧脑组织超微结构及脑组织自由基的影响。方法 将40只小鼠随机分为4组。A组为盐水对照组，B组为缺氧预处理组，IH组为缺血缺氧组，BIH组为缺氧预处理后缺血缺氧组。各组有6只小鼠分别采用黄嘌呤氧化酶法和硫代巴比妥酸法和硫巴比妥酸法检测脑组织的超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量，另4只小鼠用于透射电镜下脑组织超微结构的观察。结果 与A组比较，B组SOD活性增加，IH组MDA组含量明显增加，而IH组SOD活性明显增加的同时，MDA含量比IH明显降低。电镜显示B组除部分神经元轻度肿胀外，脑组织超微结构基本同A组，IH组细胞核变形，细胞浆成空泡，严重者满视野几乎找不到正常细胞，无损害的神经元＜10％，BIH组细胞结构基本恢复正常，无损伤神经元达63％。结论 缺氧预处理对再缺血缺氧引起的神经元损伤有保护作用，内源性抗氧化物质的增加与其有直接关系。

Effects of hypoxic pretreatment on changes in cerebral ultrastructure and free radical content induced by brain hypoxia and ischemia

Objective To investigate whether hypoxic pretreatment could ameliorate the cerebral injuries induced by brain hypoxia and ischemia Methods Forty mice weighting 18 25g were randomly allocated to 4 groups of ten mice each Group A served as control In group B animals received hypoxic pretreatment Mouse was put in a 150ml bottle, then the mouth of the bottle was closed The mouse was taken out breathing fresh air whenever it developed dyspnea When it recovered, it was put in the closed bottle again The process was repeated four times In group IH animals received ischemia/hypoxia induced by ligation of left common carotid artery and breathing 8% O 2 In group BIH animals received hypoxic pretreatment first and then ischemia/hypoxia All animals were decapitated at the end of experiment and brain was removed for ultrastrcture examination and determination of superoxide dismutase (SOD) activity and malondialdehyde (MDA) content Results In group B SOD activity increased significantly as compared with that in A group, but there was little change in MDA level In group IH MDA level was significantly higher than that in group A but there was no significant change in SOD activity In group BIH SOD activity increased but MDA decreased significantly as compared those in group IH Ultrastructure examination showed that neurons in group B were similar to those in group A except some slight swelling In group IH nucleus seriously deformed with vacuol formation in cytoplasm, less than 10% neurons were normal In group BIH neurons with normal cell structure accounted for 63% Conclusions Hypoxic pretreatment protects brain from hypoxic and ischemic injury The protection may be attributed to endogenous antioxidation