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本实验在大鼠内毒素、重度失血性休克模型上重点探讨氧自由基对肝脏亚细胞器的脂质过氧化损伤作用。结果发现,休克早期肝脏线粒体和溶酶体悬液MDA含量较对照均明显升高(P<0.05～0.01),至休克后期升高更甚(P<0.01)。休克早期肝脏线粒体悬液及溶酶体悬液SOD活力在内毒素休克时呈代偿性升高(P<0.05～0.01),以后二种休克条件下肝脏亚细胞器SOD活力均明显下降(P<0.01)。上述结果表明氧自由基在内毒素、重度失血性休克时能够引起肝脏线粒体、溶酶体等亚细胞器的脂质过氧化损伤。
This experiment focuses on the rat model of endotoxin, severe hemorrhagic shock on oxygen free radicals on liver sub-organelles of lipid peroxidation injury. The results showed that the contents of MDA in mitochondria and lysosomal suspension in the early stage of shock were significantly higher than those in the control group (P <0.05-0.01), but increased to the later stage of shock (P <0.01). The activities of SOD in mitochondrial suspension and lysosomal suspension in early stage of shock were compensatory increased in endotoxic shock (P <0.05-0.01), and the activities of SOD in liver subcellular organelles were significantly decreased after two shocks (P < 0.01). The above results indicate that oxygen free radicals can cause lipid peroxidation damage in the liver mitochondria, lysosomes and other subcellular organelles during endotoxin and severe hemorrhagic shock.