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机构地区:[1]中国医科大学附属盛京医院儿科,沈阳110004
出 处:《实用儿科临床杂志》2011年第9期691-693,共3页Journal of Applied Clinical Pediatrics
基 金:国家自然科学基金(30672253)
摘 要:目的探讨高体积分数氧(高氧)损伤状态下,新生鼠肺组织通透性及肺泡Ⅱ型上皮细胞(AECⅡ)超微结构的动态变化。方法新生大鼠320只,依据吸氧体积分数(FiO2)分组:实验组1(FiO2800 mL·L-1)、实验组2(FiO2600 mL·L-1)、实验组3(FiO2400 mL·L-1)、空气对照组(FiO2210 mL·L-1)。每组分别于实验1 d、3 d、5 d、7 d、14 d取8只鼠,计算其肺湿/干质量比值(W/D);另取8只新生鼠行支气管肺泡灌洗,检测其支气管肺泡灌洗液(BALF)中蛋白水平的动态变化;透射电镜及硝酸镧示踪技术观察其AECⅡ超微结构及细胞膜通透性改变。结果各实验组5 d、7 d、14 d肺W/D比值明显高于空气对照组,差异均有统计学意义(Pa<0.05),高氧3 d后实验组1与实验组2、实验组3的BALF中蛋白水平与空气对照组比较均显著增高(Pa<0.05);各实验组7 d内随暴露时间延长呈上升趋势;BALF中蛋白水平在实验组3、实验组2、实验组1也呈逐渐增高趋势,且与空气对照组比较均显著增高(Pa<0.05)。实验组AECⅡ的超微结构在出生后不同时间可以出现明显改变,且对硝酸镧颗粒通透性明显增加。结论高氧肺损伤早期存在肺泡上皮通透性增加导致的肺水肿改变;新生鼠随着高氧暴露浓度的增高和时间的延长,肺损伤加重。Objective To investigate the epithelial permeability in lung tissue and the ultrastructure dynamic changes of alveolar epithelia type Ⅱ cells(AEC Ⅱ) under hyperoxia-induced lung injury condition.Methods Three hundred and twenty cases of newborn rats were divided into 4 groups according to different oxygen concentrations(FiO2): experimental group 1(FiO2 800 mL·L-1),experimental group 2(FiO2 600 mL·L-1),experimental group 3(FiO2 400 mL·L-1) and room-air control group(FiO2 210 mL·L-1).Rats were killed on the 1st,3rd,5th,7th and 14th day after the onset of the experiment.The ultrastructures dynamic changes of AEC Ⅱ and alveolar barrier function through lanthanum nitrate tracing technology were observed.Lung wet/dry weight ratio(W/D) and protein content in bronchoalveolar lavage fluid(BALF) were examined.Results The lung W/D ratios in experimental groups were significantly higher than those in room-air control group on the 5th,7th and 14th day of hyperoxia exposure(Pa0.05).The protein contents of BALF in experimental groups were significantly higher than those in room-air control group(Pa0.05) and increased as the oxygen concentration elevated and exposure time prolonged.The ultrastructures of AEC Ⅱ changed dramatically with longer exposure duration and the permeability of lanthanum nitrate in experimental groups were much higher than those in room-air control group.Conclusions Increased epithelial permeability which occurred at the early stage of hyperoxia-induced lung injury can lead to pulmonary edema;the lung injury became worse with higher oxygen concentration and longer exposure duration.
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