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机构地区:[1]云南农业大学动物科技学院,昆明云南650201
出 处:《中国兽医学报》2003年第4期369-371,共3页Chinese Journal of Veterinary Science
基 金:教育部"高等学校骨干教师资助计划"资助项目 (教技司 [2 0 0 0 ] 65号 )
摘 要:将 5 6只白兔随机分成 3组 : 组为正常对照组 ,共 8只 ; 组为内毒素 (endotoxin,ET)处理组 ,共 2 4只 ; 组为阳离子 A(cation A,CA) +ET组 ,共 2 4只。 组静注等量的生理盐水 , 组静注 ET30 0 μg/ kg, 组静注 CA2 0 0 m g/kg后 ,静注 ET 30 0μg/ kg。 1、2、3、4、5 h后分别采集血液制备血浆样品。 2、5 h捕杀 组兔 4只 , 、 组兔各 12只 ,迅速采集肝脏制备组织匀浆。检测血浆 T- AOC、CAT活性和 MDA含量 ,肝 GSH、GSH- ST、GSH- Px活性。结果显示 : 组各项指标均保持相对稳定 ; 组 MDA含量比 组升高 (P<0 .0 1) , 组 MDA含量升高不显著 ; 组 T- AOC、CAT活性比 组降低 (P<0 .0 1) , 组显著高于 组 (1、2、3h,P<0 .0 1;4、5 h,P<0 .0 5 ) ; 组肝脏 GSH和 GSH- ST活性显著降低 (P<0 .0 1) ,第 5 h GSH- Px活性降低 (P<0 .0 1) ,第 2 h(P<0 .0 5 ) ; 组 GSH、GSH- Px(第 5 h显著降低 )、GSH - ST活性降低不明显。结果提示 :自由基参与了 ET休克的病理过程 。Fifty six healthy rabbits were randomly divided into three groups.The 8 rabbits in control group(groupⅠ) were infused with the same amount of 0 86% chloride sodium as in group Ⅱ.The 24 rabbits in endotoxin group(group Ⅱ) received endotoxin iv ET 300 μg/kg body weight to make the endotoxic shock model.After gave CA 200 mg/kg body weight,the 24 rabbits in ET+CA group(groupⅢ) were treated as groupⅡ.Blood simples were taken at 1,2,3,4,5 hour,for examination of the methylenedioxyamphetamine(MDA),total antioxidative capacity(T AOC) and catalse(CAT) in plasma.4 rabbits of group Ⅰ,12 rabbits of group Ⅱ and Ⅲ were killed,at 2,5 h,and their livers sampled quickly to assay the activities of glutathione(GSH),glutathione peroxidase(GSH Px) and the glutathione sulfurtransferase(GSH ST).The results were summarized as follows:all indexes of group Ⅰ had no significant change.The increase of MDA in group Ⅱ was significant(P<0 01),the plasma MDA in group Ⅲ increased not as high as group Ⅱ,and there wasn′t significant difference between group Ⅰ and Ⅲ.Plasma CAT and T AOC of group Ⅱ decreased significantly(P<0 01),and group Ⅲ decreased lower than group Ⅱ.The activities of liver GSH,GSH Px and GSH ST in group Ⅱ reduced markedly(P<0 01).All indexes of group Ⅲ were higher than those in group Ⅱ,except GSH Px at 5 h.The results showed that CA can effectively counteract the injury of the lipid peroxidation by endotoxin induced free radical.
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