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地塞米松对其影响。方法 :30只SD大鼠随机分成对照组、ET组、ET +地塞米松组 ,静脉注射内毒素 (2 0 0 μg/kg)造成急性肺损伤。结果 :4h后血浆和肺组织匀浆中NO2 -/NO3 -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 ,与对照组相比差异有显著性 (P <0 0 5或P <0 0 1) 。注射内毒素前 1h静脉注射地塞米松 (70mg/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 ,地塞米松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 its effect on dexamethasone. Methods: Thirty SD rats were randomly divided into control group, ET group and ET + dexamethasone group. Intravenous endotoxin (200 μg / kg) caused acute lung injury. Results: After 4h, NO2 - / NO3 - and MDA content, pulmonary coefficient, lung water content and relative humidity of lung and lung were significantly increased in plasma and lung homogenate, compared with the control group Significance (P <0.05 or P <0.01). One hour before injection of endotoxin, dexamethasone (70mg / kg) significantly attenuated endotoxin-induced lung injury, inhibited endotoxin-induced NO-2 / NO-3 and MDA levels and lung coefficient, There was a positive correlation between the relative humidity and relative humidity, the content of NO-2 / NO-3 and the content of MDA in plasma and lung. CONCLUSION: NO mediates endotoxin-induced lung injury. NO released in large quantities is involved in lipid peroxidation of lung injury. The protective effect of dexamethasone on lung injury may be related to the reduction of NO release and anti-lipid peroxidation.