中国实验动物学报
中國實驗動物學報
중국실험동물학보
ACTA LABORATORIUM ANIMALIS SCIENTIA SINICA
2015年
4期
347-352
,共6页
酸吸入%肺损伤%气管插管%模型%小鼠
痠吸入%肺損傷%氣管插管%模型%小鼠
산흡입%폐손상%기관삽관%모형%소서
Acid aspiration%Lung injury%Orotracheal intubation%Model%C57BL/6 mice
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C57 BL／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、pH 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。
目的：建立一種無創傷、可進行縱嚮研究的痠吸入導緻肺損傷的小鼠模型。方法痳醉後的C57 BL／6小鼠利用光纖光源引導進行口腔氣管插管，配閤側臥體位及施壓小鼠左肺，嚮其右側肺部分彆導入2.5μL／g、0.1 mol／L、pH 1.5的鹽痠或對照生理鹽水。手術完成後對小鼠進行供氧4 h恢複。手術後對小鼠的存活率及肺功能生理指標進行鑑測，確定肺損傷後小鼠病程髮展各項檢測指標。結果經上述方法建立的無創傷痠吸入小鼠，染色顯示液流成功導入小鼠右側肺部，存活率（80％）顯著高于氣管切口插管的小鼠。肺功能檢測（濕榦重比、迴彈性、動脈血氧飽和度）和組織學切片錶明，鹽痠的導入引起小鼠肺部嚴重病理反應和功能障礙。對小鼠肺盥洗液分析揭示痠吸入導緻大量嗜中性粒細胞進入肺泡，併可在肺泡中檢測到高含量免疫炎性因子TNF-α、IL-6、CXCL1和CXCL2。結論採用可視化無創傷的口腔氣管插管技術，同時灌註鹽痠所建立的痠吸入肺損傷小鼠模型，為進一步研究肺部免疫炎癥機理提供瞭平檯。
목적：건립일충무창상、가진행종향연구적산흡입도치폐손상적소서모형。방법마취후적C57 BL／6소서이용광섬광원인도진행구강기관삽관，배합측와체위급시압소서좌폐，향기우측폐부분별도입2.5μL／g、0.1 mol／L、pH 1.5적염산혹대조생리염수。수술완성후대소서진행공양4 h회복。수술후대소서적존활솔급폐공능생리지표진행감측，학정폐손상후소서병정발전각항검측지표。결과경상술방법건립적무창상산흡입소서，염색현시액류성공도입소서우측폐부，존활솔（80％）현저고우기관절구삽관적소서。폐공능검측（습간중비、회탄성、동맥혈양포화도）화조직학절편표명，염산적도입인기소서폐부엄중병리반응화공능장애。대소서폐관세액분석게시산흡입도치대량기중성립세포진입폐포，병가재폐포중검측도고함량면역염성인자TNF-α、IL-6、CXCL1화CXCL2。결론채용가시화무창상적구강기관삽관기술，동시관주염산소건립적산흡입폐손상소서모형，위진일보연구폐부면역염증궤리제공료평태。
Objective To establish a non-traumatic mouse model of acid aspiration-induced lung injury which al-lows longitudinal studies.Method C57BL/6 mice were anesthetized and orotracheally intubated with a 20 gauge angio-catheter guided by optical fiber.The mice were subsequently placed in the right lateral decubitus position and external com-pression to the left lung was manually applied.A polyethylene catheter was advanced into the right lung and used to instill either hydrochloric acid (2.5μL/g, 0.1 mol/L, pH 1.5) or saline as control.Then the mice were recovered with supple-mental oxygen for 4 hours.The pulmonary physiological function and survival of mice within 2 weeks after surgery were as-sessed.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 oxy-gen 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 bronchoalve-olar 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.
