目的　探讨冲击波、四氧化二氮 (N2 O4 )及其复合效应所致大鼠肺组织损伤特点 ,c- fos基因表达及其意义。　方法　采用雄性 Wistar大鼠复制冲击伤、N2 O4 中毒及复合效应动物模型 ,于伤后 3、6、12、2 4、4 8及 72 h活杀 ,采用苏木精伊红及标记的抗生蛋白链菌素生物素免疫组织化学技术观察肺组织损伤病变特点及 c- fos基因表达的变化。　结果　冲击伤组肺组织出血 (3h)、水肿和透明膜形成 (6 h)、炎细胞浸润 (1～ 3d) ,并见大量单核细胞 (2 d)及泡沫样细胞 (3d)。N2 O4 组肺组织于伤后 3h见水肿、渗出 ,6～ 12 h见多量的嗜酸性粒细胞和单核细胞 ,1～ 3d见大量的单核细胞和泡沫样细胞。冲击伤 +N2 O4 组肺组织出血水肿严重 ,炎细胞渗出早而多 ,支气管阻塞严重。免疫组织化学显示 c- fos蛋白于冲击伤组和 N2 O4 组表达均明显增加 ,而于冲击伤 +N2 O4 组表达持续呈强阳性 ,其阳性部位以支气管上皮、血管内皮和单核细胞为主。　结论　冲击波和 N2 O4 均可引起大鼠肺组织出血、水肿、炎细胞浸润、水肿吸收和退变吞噬等病理变化 ;冲击伤合并 N2 O4 中毒使肺组织损伤出现叠加效应 ;c- fos基因表达可能在冲击波和 N2 O4 致肺损伤的发生、发展过程中起一定的作用 Objective To investigate the characteristics of lung injury, c-fos gene expression and their significance in rats induced by shock wave, nitrogen tetraoxide (N 2 O 4) and their combined effect. Methods Male Wistar rats were used to replicate the animal models of impact injury, N2 O4 poisoning and combined effects. The animals were sacrificed at 3, 6, 12, 2, 4, 8 and 72 h after injury. Erythromycin Eosin and labeled anti- Streptavidin biotin immunohistochemistry was used to observe the pathological changes of lung tissue and the changes of c-fos gene expression. Results The hemorrhagic lung tissue (3 h), edema and hyaline membrane formation (6 h) and infiltration of inflammatory cells (1 ~ 3 d) were observed in the injured group. A large number of mononuclear cells (2 d) and foamy cells (3 d) were observed. The lung tissue of N2 O4 group showed edema and exudation at 3h after injury. A large amount of eosinophils and mononuclear cells were seen at 6 ~ 12 h. A large number of mononuclear cells and foamy cells were observed at 1 ~ 3d. Blast injury + N2 O4 group of severe pulmonary hemorrhage edema, inflammatory cells exudate earlier and more, bronchial obstruction. Immunohistochemistry showed that the expression of c-fos protein in the injured group and N2 O4 group were significantly increased, while in the injury + N2 O4 group showed a strong positive expression of the positive parts of the bronchial epithelium, vascular endothelial cells and monocytes . Conclusion Both shock wave and N2 O4 can cause pathological changes of hemorrhage, edema, inflammatory cell infiltration, edema absorption and degeneration and phagocytosis of lung tissue in rats. Impact injuries with N2 O4 poisoning may cause superposition of lung injury; c-fos gene expression may In the shock wave and N2 O4 induced lung injury, the development process play a role