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多系统器官衰竭的氧自由基机制 被引量:17

Oxygen free radical mechanism in multiple system organ failure
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摘要 本文用单核吞噬细胞系统封闭加出血性休克造成多系统器官衰竭(MSOF)的大鼠,探讨乳自由基在其发生中的作用。渡过休克后发生MSOF的动物,全血还原型谷胱廿肽(GSH)在第二天升高,为4.17±0.38mg/gHb(基础值为2.67±0.09)。血浆谷胱甘肽过氧化物酶第1天下降最多(1.22±0.27U/ml·min),第2、3天渐升,仍低于基础值3.08±0.200。全血超氧化物歧化酶(SOD)一直低于基础值249.5±72.4μg/gHb,第1天达182.6±27.1。血浆丙二醛高达基础位(6.54±0.31nmol/ml)的2倍。相关检验表明,MSOF大鼠的肺系数、血浆GPT和肌酐分别与肺,肝匀浆SOD及肾GSH水平呈负相关。结果提示MSOF时血和组织中抗氧化剂、抗氧化酶和脂质过氧化物水平有明显变化,器官衰竭似与组织的抗氧化能力下降有关。 The role of oxygen free radicals in multiple system organ failure (MSOF) was studied in rats produced by reticuloendothelial system blockade in addition to hemorrhagic shock. In MSOF animals blood reduced glutathione (GSH) elevated to 4.17±0.38 mg/g Hb at day 2, compared with baseline 2.67±0.09. Plasma glutathione peroxidase declined to 1.22±0.27 U/ml·min at day 1, and gradually increased at day 2 and day 3, but still lower than baseline 3.08±0.20. Blood superoxide dismutase (SOD) level was 182.6±27.1 at day 1, lower than baseline 249.5±72.4 μg/g Hb. Plasma malondialdehyde (MDA) increased twice the normal level of 6.54±31 nmol/ml. Correlation analysis showed that lung index, plasma GPT and creatinine negatively correlated with the level of lung and liver homogenate SOD and kidney homogenate GSH, respectively.Results indicate that there are significant changes in the levels of blood and tissue antioxidants and lipid peroxides during MSOF. Organ failure appears to be correlated with the decrease in tissue antioxidation capacity.
出处 《中国病理生理杂志》 CAS CSCD 北大核心 1990年第4期203-206,共4页 Chinese Journal of Pathophysiology
关键词 多器官衰竭 休克 氧自由基 Multiple organ failure Shock, hemorrhagic Free radicals
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参考文献3

  • 1刘智峰,方允中.血液中超氧化物歧化酶测定的光化学扩增法[J]军事医学科学院院刊,1986(04).
  • 2齐凤菊,周玫,陈瑗,孔华.血浆丙二醛含量的测定方法—改良的八木国夫法[J]第一军医大学学报,1986(02).
  • 3C. Ritter MD,R. A. Hinder FRCS, PhD,M. M. J. Oosthuizen PhD,L. G. Svensson FRCS, PhD,S. J. S. Hunter BSc (HONS),H. Lambrecht BSc. Gastric mucosal lesions induced by hemorrhagic shock in baboons[J] 1988,Digestive Diseases and Sciences(7):857~864

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