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作 者:李端祥[1] 欧阳静萍[1] 常江[1] 涂淑珍[1] 杨海鹭[1] 邓冠斌[1] 董传仁[1] 刘志军 夏仕雄 郑信华
机构地区:[1]湖北医科大学病理生理学教研室,武汉冶金医学专科学校
出 处:《微循环学杂志》1994年第1期10-11,F002,共3页Chinese Journal of Microcirculation
摘 要:采用犬失血性休克输血复苏模型,观察了硫氮酮(Diltiazem,DZ)对休克犬肝、肾、心、肺4个器官组织超微结构及组织中丙二醛(MDA)含量和黄嘌呤氧化酶(XO)活性的影响。结果显示:DZ可使休克犬各器官组织超微结构的损伤性改变明显减轻;DZ处理组各器官组织中MDA含量和XO活性均显著低于对照组。表明DZ对失血性休克犬多个器官具有保护作用,该效应与其抑制XO活性和氧自由基介导的脂质过氧化反应有关。The effects of diltiazem on ultrastructure and lipid peroxidation in the liver,kidney,heart and lung of the dogs with hemorrhagic shock were studied.Anesthetized mongrel dogs were rapidly bled to a mean blood pressure of 6.0kpa and maintained at that level for 90min followed by resuscitation with all shed blood.At 30 min into hemorrhagic shock,diltiaxem(40μg/kg·min,n=6) or same volume of saline(3ml/kg,n=5) was infused intravenously iver 15min.At 159min after resuscitation,the dogs were euthanized and tissue samples were obtained and analysised.The results showed that diltiazem significantly ameliorate the damage ultrastructural in all tissue from the organs observed. Samples from the organs of diltiazem treated dogs exhibited less malondialdehyde and lower xanthin oxidase activity as compared with those of control dogs.These data suggest that diltiazem has a protective effect on mulit-organs of hemcrrhagic dogs and which is related to it's inhibition on lipid peroxidation in tissue.
关 键 词:脂质过氧化 失血性休克 超微结构 硫氮革酮 多器官功能衰竭 多器官功能障碍 Radical 组织细胞损伤 CA^++ 氧自由基 致休克 钙内流 细胞内
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