目的　探讨吸入NO对在体兔肺缺血再灌注损伤时的作用及机理。材料与方法　将 3 2只日本大白兔随机分为 4组 ,每组 8只 ,其中对照组仅作剖胸手术 ,无肺缺血再灌注 ;缺血再灌注组则在剖胸后结扎左肺动脉造成左肺缺血、停通气 2h ,继之开放左肺动脉、正常通气观察 2h ;吸入NO组分为 2组 ,分别在再灌注第 11min开始吸入 2 0ppm或 60ppmNO ,连续 3 0min。在术前及再灌注后监测Pa0 2、cGMP、slCAM -1、XOD和MDA ,并在再灌注 2h测左肺含水量及组织学检查。结果　显示再灌注后Pa0 2 、cGMP降低 ,sICAM -1、XOD、MDA及肺含水量增加 ,肺泡内明显渗出 ,肺泡II型上皮细胞及血管内皮细胞明显受损 ;而吸入 2 0或 60PPMNO能使cGMP含量恢复 ,肺形态和功能受损明显减轻。结论　肺在体缺血 2h ,再灌注 2h可形成明显的肺损伤 ,吸入NO能通过升高cGMP而对肺缺血再灌注损伤起保护作用。 Objective To investigate the effect and mechanism of inhaled NO on lung ischemia-reperfusion injury in rabbits. Materials and Methods 32 Japanese white rabbits were randomly divided into 4 groups with 8 rats in each group. The control group was only used for thoracotomy and no ischemia / reperfusion. The ischemia-reperfusion group was ligated left thoracotomy after thoracotomy Left lungs were ventilated for 2 hours, then left pulmonary artery was opened and normal ventilation was observed for 2 hours. Inhalation of NO was performed in 2 groups, and inhaled 20ppm or 60ppm NO respectively at the 11th minute after reperfusion for 30min continuously. PaO2, cGMP, slCAM-1, XOD and MDA were monitored before and after reperfusion. Left lung water content and histological examination were performed 2h after reperfusion. The results showed that PaO 2, cGMP decreased, sICAM -1, XOD, MDA and lung water content increased significantly after reperfusion, alveolar effusion, type II alveolar epithelial cells and vascular endothelial cells significantly damaged; while inhaled 20 or 60PPMNO energy So cGMP content recovery, lung morphology and function was significantly reduced. Conclusion Pulmonary lung injury can cause obvious lung injury at 2h after ischemia and 2h after reperfusion. Inhaled NO can protect lung against ischemia-reperfusion injury by increasing cGMP.