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大鼠内毒素休克30min,心、肺、肠组织MDA较对照明显升高(P<0.05),心、肝、肾、肠组织SOD呈代偿性升高(P<0.05),但肺组织SOD明显抑制(P<0.05)。休克后2h,心、肝、肾、肺、肠组织MDA显著升高(P<0.05～0.001),此时除肝、肾组织SOD仍代偿性升高外,心、肺、肠组织SOD呈抑制状态。休克后4h,5个测定生命器官组织MDA升高更甚(P<0.01～0.001),而SOD均呈明显抑制(P<0.05～0.01)。结果表明内毒素休克时氧自由基介导的脂质过氧化反应导致了各生命器官的组织损伤,其中以心、肺、肠器官发生最早,组织内源性SOD活力在休克后期明显受抑。
The level of MDA in heart, lung and intestine was significantly higher than that in control (P <0.05), SOD in heart, liver, kidney and intestine was compensatory increased (P <0.05) Significant inhibition (P <0.05). At 2h after shock, MDA in heart, liver, kidney, lung and intestine increased significantly (P <0.05-0.001). At this time, SOD in heart, lung and intestine was increased Inhibit the state. 4 h after shock, the MDA levels in vital organs were even higher (P <0.01 ~ 0.001), while SOD was significantly inhibited (P <0.05 ~ 0.01). The results showed that endogenous oxygen-mediated lipid peroxidation induced endotoxin-induced tissue damage in all organs of life, including the earliest heart, lung and intestine organs, tissue endogenous SOD activity was significantly inhibited in the late shock.