创伤性休克时自由基对5个重要器官及肝线粒体的损伤作用

Injurious effects of free radicals on 5 organs and hepatic mitochondria during traumatic shock in rats

一侧股骨粉碎性骨折伴失血15％体重之大白鼠,致伤后1h,心、肺组织MDA明显升高(P<0.05),肺组织SOD明显下降(P<0.05),肝线粒体悬液MDA和SOD呈同步显著升高(P<0.05)。致伤后3h,心、肝、肾、肺组织MDA升高更甚(P<0.01),心、肾、肠组织SOD亦升高(P<0.05～0.01),肝线粒体悬液MDA更为升高(P<0.01),而SOD则出现下降(P<0.05)。致伤后5h,5个测定器官组织MDA均升高显著(P<0.01～0.001),而SOD均呈下降趋势(P<0.01～0.001),此时肝线粒体悬液MDA和SOD反相变化更甚(P<0.01～0.001)。血浆MDA随致伤时间延长而逐渐增高(P<0.05～0.001),溶血液SOD逐步下降(P<0.05～0.01),反映溶酶体破裂的血浆β-葡萄糖醛酸酶和酸性磷酸酶亦随致伤时间而增高(P<0.05-0.001)。上述结果证实大白鼠创伤性休克时氧自由基对细胞和肝线粒体的损伤作用。

A model of traum a shook was established in rats by comminutedly fracturing of the right femur and bleeding of 15% of the body weight.In the 1st hour after injury,the content of malondialdehyde (MDA) of the heart and the lungs increased,the activity of sv.peroxide dismutase (SOD) in the lungs decreased,and the MDA content and SOD activity in hepatic mitochondria increased synchronously.In the 3rd hour after injury,the MDA content increased not only in the heart,the lungs and hepatic mitochondria but also in the liver and the kidneys,and the SOD activity increased in the heart,the kidneys and the intestinal tract but decreased in hepatic mitochondria.There were further marked elevation of MDA content and progressive inhibition on SOD activity in the 5 vital organs and hepatic mitochondria in the 5th hour after injury.When shock continued to progress,the plasma MDA content increased gradually,the SOD activity of the hemolytic blood decreased,and the activities of plasma acid phosphatase and β-glucuronidase,the indicators of lysosome destruction,increased markedly.These findings suggest that the oxygen-derived free radicals are responsible for the damages to cells of the vital organs and subcellular organelles during traumatic shock.