中文摘要：

为探讨自由基在山羊内毒素血症发病机理中的作用，将48只山羊随机分为A、B、C、D共4组，每组12只，A组为对照组，B组为内毒素组，C组为氨基胍治疗组，D组为氨基胍组。其中每组又分成注射LPS后3h测定组与注射LPS后6h测定组每组12只。分别在处理后3h和6h每组各宰杀6只提取心肌线粒体，检测心肌线粒体中的总抗氧化能力（T—AOC）、超氧化物歧化酶（SOD）和过氧化氢酶（CAT）活性以及丙二醛（MDA）含量的变化。结果显示，内毒素血症时山羊心肌线粒体中SOD，T—AOC和CAT活性降低，MDA含量明显升高，而氨基胍治疗组则情况明显好转。结果表明，由于自由基的增多而引起的脂质过氧化损伤在山羊内毒素血症发病机理中起着重要的作用，氨基胍可有效拮抗脂质过氧化造成的损伤。

英文摘要：

To explore the role of free radical on pathogenesis of endotoxemia in goats ,48 goats were divided randomly into 4 groups of A , B , C and D with 12 goats in each group. Group A was the normal control ; Group B was the LPS group ; Group C was the LPS ＋ AG group ; Group D was the AG group, each of which was divided into 3h slaughter group after the injection of LPS and 6h group after injection of LPS. The changes of the total antioxidant capacity （ T - AOC） , superoxide dismutase （SOD） and catalase （CAT） activity and the content of MDA in myocardial mitochondria were detected. The results showed that when the goat caught endotoxemia the activity of SOD, T - AOC and CAT in myocardial mitochondrial reduced, MDA increased significantly. Compared with the Lps group the situation of aminoguanidine treatment group was significantly improved. The results indicated that, lipid peroxidation damage in the goat caused by the over -produced free radicals played an important role in the pathogenesis of endotoxemia. Aminoguanidine can effectivly antagonize lipid peroxidation damage.