摘要
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。
The effects of nitric oxide (NO) on intestinal damage were observed after treatment with Nw- nitro - L - arginine (L - NNA), an inhibitor of NO synthase,or L - arginine (L - Arg), the substrate for NO synthase, in an endotoxemic rat model. The results showed that inhibition of NO production with L - NNA (4mg/kg)aggravated the endotoxin (ET, 10mg/kg) induced intestinal microvascular and mucosal damage, which were shown by the increase of intestinal Evan's blue content and decrease of diamine oxidase activity.Moreover,the intestinal myeloperoxidase and malondialdehyde were significantly increased, and the blood flow decreased. Administration of L - Arg (40mg/kg), however, had the opposite effects. It is suggested that NO may have a protective effect on intestine during endotoxemia, and the mechanisms might be mediated by inhibition of accumulation of leukocyte,decreasing free radical injury and improving the intestinal blood perfusion.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1997年第6期677-680,共4页
Chinese Journal of Pathophysiology
