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目的 探讨诱导型一氧化氮合酶 (iNOS)在急性肺损伤 (ALI)发病中的作用及吸入一氧化氮对肺损伤的影响。方法 以内毒素和油酸复制大鼠ALI模型 ,随后对肺损伤大鼠进行低剂量一氧化氮 (NO)吸入治疗 ,同时以生理盐水作对照。应用免疫组织化学方法和图像分析系统 ,检测实验组肺组织中iNOS表达。结果 实验组iNOS表达为 :生理盐水组和NO对照组为 63 .3 3± 2 6.65和 42 .89± 2 8.91;内毒素和油酸ALI模型组为 176.44± 2 1.47和 176.5 6± 2 8.71;内毒素和油酸模型的NO治疗组为 78.11± 2 1.66和 83 .78± 44 .3 ;两个模型组与对照组和NO治疗组比较差异有显著性(P <0 .0 1)。结论 iNOS在ALI发病中起着重要作用 ,吸入小剂量外源性NO ,对缓解ALI有一定的作用
Objective To investigate the role of inducible nitric oxide synthase (iNOS) in the pathogenesis of acute lung injury (ALI) and the effect of inhaled nitric oxide on lung injury. Methods Rat ALI model was induced by lipopolysaccharide (LPS) and oleic acid, followed by low-dose inhaled nitric oxide (NO) inhalation for rats with lung injury. Meanwhile, saline was used as a control. Immunohistochemistry and image analysis system were used to detect iNOS expression in the experimental group. Results The expression of iNOS in the experimental group was 63.33 ± 2 6.65 and 42.89 ± 2.891 in the saline group and NO control group, 176.44 ± 2 1.47 and 176.5 6 ± 2 8.71 in the endotoxin and oleic ALI model groups, respectively. The endotoxin and oleic acid NO treatment groups were 78.11 ± 2 1.66 and 83.78 ± 44.3, respectively. There were significant differences between the two model groups and the control group and NO treatment group (P <0.01). Conclusion iNOS plays an important role in the pathogenesis of ALI. Inhalation of low dose of exogenous NO may play a role in alleviating ALI