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本文用一氧化氮（NO）合酶抑制剂硝基左旋精氨酸（L-NNA）及其底物左旋精氨酸（L—Arg）对比观察了两者对内毒素血症大鼠肠道损伤的影响，并从白细胞、自由基及血流改变等方面探讨了其作用机理。结果表明，用L—NNA（4mg／kg）抑制NO合成可加重内毒素（10mg／kg）引起的肠微血管和粘膜损伤，表现为肠组织伊文氏蓝含量增加，二胺氧化酶活性降低，同时肠组织髓过氧化物酶及两二醇含量明显升高，肠血流降低：用L-Arg（40mg/kg）促进NO合成则减轻上述改变。提示NO在内毒素血症时具有保护肠道的作用，其机理与减少肠组织白细胞集聚、降低脂质过氧化损伤和改善肠血流等有关。
In this paper, nitric oxide (NO) synthase inhibitor nitro-L-arginine (L-NNA) and its substrate L-arginine (L-Arg) compared the two endotoxemia rat intestine Injury, and from the white blood cells, free radicals and changes in blood flow and other aspects of its mechanism of action. The results showed that inhibition of NO synthesis with L-NNA (4 mg / kg) aggravates intestinal microvascular and mucosal injury induced by endotoxin (10 mg / kg), with an increase of intestinal Evans blue and a decrease of diamine oxidase activity Intestinal myeloperoxidase and two diol content was significantly increased intestinal blood flow decreased: L-Arg (40mg / kg) to promote NO synthesis while reducing the above changes. Tip NO in the endotoxemia has the role of protecting the intestine, its mechanism and reduce the intestinal white blood cell aggregation, reduce lipid peroxidation damage and improve intestinal blood flow and so on.