目的:建立改良大鼠肺再灌注(IR)损伤模型，评估其病理生理表现，探讨其可行性和重复性。方法:28只成年SD大鼠，每组14只，随机分为假手术组(SHAM组)和肺IR损伤组(IR组)。IR组全麻下气管切开机械通气，仰卧位开胸，找到解剖标志物支气管软骨，暂停通气并置入止血夹，恢复通气，阻断肺门30 min后开放IR 45 min。SHAM组全麻下气管切开机械通气，分离肺门相同时间后关胸。术后抽取动脉血气，肺组织进行大体及HE染色，观察病理改变，测定干湿比，并用Western Blot法检测肺组织中氧化应激通路p38MAPK及NF-κB信号通路、炎性因子TNF-α、内皮细胞功能标志物eNOS表达水平。结果:肺IR损伤可见气管内粉红色水样分泌物，肺大体呈水肿、淤血征象。肺泡炎评分显著升高，干湿比升高，伴p38MAPK、NF-κB信号通路激活，TNF-α表达显著升高，eNOS表达显著下降。结论:左侧夹闭肺门、双侧IR损伤模型是一种实用动物模型，该改良手术方法操作简单、成本低，安全性及可重复性高。“,”Objective:In this study, we established a reliable surgical procedure of lung ischaemia-reperfusion(IR) injury in rats. The research progress of different lung IR injury models and application value was also discussed.Methods:Twenty-eight adult SD rats were randomly divided into SHAM group and lung IR injury group(IR group), 14 rats in each group. In IR group, rats underwent tracheotomy under general anesthesia and received mechanical ventilation. Chest was opened in supine position, and pulmonary hilum was blocked for 30 minutes then the occlusion was removed. Samples were harvested after reperfusion for 45minutes. Rats in SHAM group received surgery and exposure of the right pulmonary artery, and experienced the same amount of time before the chest closed. Arterial blood gas was extracted postoperatively. Gross view of the lungs and pathological changes were observed, and the dry/wet ratio(W/D) was determined. Protein level of pro-inflammatory factors, markers in oxidative stress pathway, and endothelial functional markers in lung were tested by western blot analysis.Results:In IR group, there was pink foamy secretion in the airway, and the lungs exhibited signs of edema and congestion. In IR group, the alveolitis score was significantly increased, the W/D ratio was also increased, p38MAPK and NF-κB signaling pathways were activated, and the expression of TNF-α was significantly increased, while the expression of eNOS was significantly decreased.Conclusion:Left hilum clamping and bilateral reperfusion injury in lung is a practical animal model, it is a simple, low-cost and repeatable animal model for further studies. No microsurgical instruments were required during the procedure. Lung IR injury is characterized by oxidative stress response, inflammatory response and endothelial cell dysfunction.