论文部分内容阅读
目的：探讨内毒素型肺损伤与一氧化氮的关系及山莨菪碱对其影响。方法：３０ 只ＳＤ 大鼠随机分成对照组、ＥＴ组、ＥＴ＋ 山莨菪碱组，静脉注射内毒素（２００ μｇ／ｋｇ） 造成急性肺损伤。结果：４ ｈ 后血浆和肺组织匀浆中ＮＯ－２ ／ＮＯ－３ 含量和丙二醛（ＭＤＡ） 含量、肺系数、肺含水量、肺干湿相对密度均显著升高，与对照组比较差异有显著性（ Ｐ＜０ ．０５ 或Ｐ＜０ ．０１），注射内毒素后５ ｍｉｎ、２ ｈ 静脉注射山莨菪碱（５ｍｇ／ｋｇ）可明显减轻内毒素引起的肺损伤，抑制内毒素引起的ＮＯ－２ ／ＮＯ－３ 含量和ＭＤＡ 含量及肺系数、肺含水量、肺干湿相对密度的升高；血浆、肺组织中ＮＯ－２ ／ＮＯ－３ 含量与ＭＤＡ含量呈正相关。结论：ＮＯ 介导了内毒素型肺损伤，大量释放的ＮＯ参与肺损伤的脂质过氧化反应，山莨菪碱保护肺损伤作用可能与降低ＮＯ 释放、抗脂质过氧化有关。
Objective: To investigate the relationship between endotoxin-induced lung injury and nitric oxide and the effect of anisodamine on it. Methods: Thirty SD rats were randomly divided into control group, ET group, ET + anisodamine group and intravenous injection of endotoxin (200 μg / kg) to induce acute lung injury. Results: After 4 h, NO-2 / NO-3 content and MDA content, lung coefficient, lung water content and relative humidity of lung and lung in plasma and lung homogenate were significantly increased compared with control group The difference was significant (P <0.05 or P <0.01). An intravenous injection of anisodamine (5 mg / kg) 5 min after injection of endotoxin could significantly reduce endotoxin-induced lung injury and inhibit endotoxin NO-2 / NO-3 content and MDA content as well as pulmonary coefficient, lung water content and relative density of lung wet and dry. The content of NO-2 / NO-3 in plasma and lung tissue was positively correlated with MDA content. CONCLUSION: NO mediates endotoxin-induced lung injury. NO released in large quantities is involved in lipid peroxidation of lung injury. Anisodamine may protect lung from injury by decreasing NO release and anti-lipid peroxidation.