【摘要】 目的建立一种无创伤、可进行纵向研究的酸吸入导致肺损伤的小鼠模型。方法麻醉后的C57BL/6小鼠利用光纤光源引导进行口腔气管插管,配合侧卧体位及施压小鼠左肺,向其右侧肺部分别导入2.5μL/g、0.1 mol/L、p H 1.5的盐酸或对照生理盐水。手术完成后对小鼠进行供氧4 h恢复。手术后对小鼠的存活率及肺功能生理指标进行监测,确定肺损伤后小鼠病程发展各项检测指标。结果经上述方法建立的无创伤酸吸入小鼠,染色显示液流成功导入小鼠右侧肺部,存活率(80%)显著高于气管切口插管的小鼠。肺功能检测(湿干重比、回弹性、动脉血氧饱和度)和组织学切片表明,盐酸的导入引起小鼠肺部严重病理反应和功能障碍。对小鼠肺盥洗液分析揭示酸吸入导致大量嗜中性粒细胞进入肺泡,并可在肺泡中检测到高含量免疫炎性因子TNF-α、IL-6、CXCL1和CXCL2。结论采用可视化无创伤的口腔气管插管技术,同时灌注盐酸所建立的酸吸入肺损伤小鼠模型,为进一步研究肺部免疫炎症机理提供了平台。更多还原

【Abstract】 Objective To establish a non-traumatic mouse model of acid aspiration-induced lung injury which allows longitudinal studies. Method C57 BL /6 mice were anesthetized and orotracheally intubated with a 20 gauge angiocatheter guided by optical fiber. The mice were subsequently placed in the right lateral decubitus position and external compression to the left lung was manually applied. A polyethylene catheter was advanced into the right lung and used to instill either hydrochloric acid( 2. 5 μL / g,0. 1 mol / L,p H 1. 5) or saline as control. Then the mice were recovered with supplemental oxygen for 4 hours. The pulmonary physiological function and survival of mice within 2 weeks after surgery were assessed. Results Methylene blue instillation showed that the staining fluid went into the right lung of the non-traumatically intubated mice. The survival rate of the mice with non-traumatic instillation was 80%,statistically significantly higher than those with tracheostomy instillation. Histological examination and lung function( wet / dry ratio,elastance and arterial oxygen saturation) assay demonstrated that acid instillation caused a profound pathological changes and functional impairment of the lung. Besides,acid aspiration into the mouse lung caused a significant increase in neutrophil infiltration in mouse pulmonary alveoli and high concentrations of inflammatory factors( TNF-α,IL-6,CXCL1 and CXCL2) in the bronchoalveolar lavage fluid. Conclusions We successfully established a mouse model of acid aspiration-induced lung injury,which may serve as a reliable model for longitudinally studying pulmonary immune-inflammatory mechanism in humans.更多还原