文档介绍：EPO对失血性休克合并内毒素血症兔TNFα、IL6、IL10、MDA影响的研究
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【摘要】[目的]观察内毒素血症引起兔脂质过氧化产物、炎症因子水平改变,运用促红细胞生成素(EPO)进行干预。[方法]兔股动脉放血造休克随后复苏,予腹腔注射内毒素,两次打击造成兔多脏器功能不全模型;24只健康新西兰大白兔随机分成对照组、二次打击组、EPO组,每组8只;造模前后留取血标本用于检测TNFα、IL6、IL10、MDA等指标。[结果]二次打击致其它两组MDA水平明显高于对照组,EPO组MDA水平较二次打击组明显降低;二次打击致其它两组TNFα、IL6、IL10水平明显高于对照组,EPO组明显低于二次打击组。[结论]TNFα,IL6,IL10等炎症因子与MDA等脂质过氧化产物参与了失血性休克合并内毒素血症所致多脏器损伤的过程,EPO能降低失血性休克合并内毒素血症兔炎症因子及脂质过氧化产物水平。
【关键词】内毒素血症;促红细胞生成素;多脏器功能不全;炎症因子
Abstract: [O
bjective]To explore the rabbits’ lipid peroxidation and cytokine level change caused by endotoxemia,use EPO for intervention.[Method]Bleed rabbits femoral for shock,ing to,make injection of endotoxin,two beatings make dysfunctional ans model;randomly divide 24 healthy rabbits into control group(1),2beating group(2),EPO group(3),8 in each;take blood for testing indexes of TNFα,IL6,IL10 and MDA.[Result]Group 2 was higher than other groups on MDA level,group 3 less than group 2;group 2 was much higher than other 2 groups on TNFα,IL6 and IL10,group 3 less than group 2.[Conclusion]The cytokines and lipid peroxidation participating in the course of an injury caused by blood loss shock and endotoxemia can be reduced by EPO.
Key words: endotoxemia;EPO;dysfunctional ans;cytokines
严重的内毒素血症引起休克、DIC,甚至多器官功能衰竭(MODS)。促红细胞生成素(erythropoietin,EPO)是一种刺激骨髓造血的糖蛋白类激素,主要由肾脏皮质、髓质交界处的肾小管旁细胞分泌,。由于其