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宋立成,程浩,奂剑波,陈丽娜,韩志海.模拟舰船火灾烟雾吸入致急性肺损伤大鼠模型的建立与评估[J].中国实验动物学报,2018,26(5):631~638.
模拟舰船火灾烟雾吸入致急性肺损伤大鼠模型的建立与评估
Assessment of a rat model of battleship fire?related smoke inhalation injury
投稿时间:2018-03-30  
DOI:10.3969/j. issn. 1005 - 4847. 2018. 05. 015
中文关键词:  烟雾吸入性肺损伤  模型  肺泡灌洗液  巨噬细胞
英文关键词:smoke inhalation?induced lung injury  model  bronchoalveolar lavage fluid  macrophage
基金项目:
作者单位E-mail
宋立成 中国人民解放军海军总医院呼吸与危重症医学科,北京 100048 songlicheng@ tom. com 
程浩 中国人民解放军海军总医院呼吸与危重症医学科,北京 100048  
奂剑波 中国人民解放军海军总医院呼吸与危重症医学科,北京 100048  
陈丽娜 中国人民解放军海军总医院呼吸与危重症医学科,北京 100048  
韩志海 中国人民解放军海军总医院呼吸与危重症医学科,北京 100048 hanzhihai@ sohu. com 
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中文摘要:
      目的 建立一种以多种复合材料为燃烧物,且温度可控的舰船火灾烟雾吸入性急性肺损伤大鼠模型?方法 设计独立的产烟箱与舱室模拟箱,将清醒的大鼠限制在舱室模拟箱体内指定区域的鼠笼内?实验过程中通过检测并控制试验箱内进烟量达到致伤因素稳定的目的?实验分两部分进行,第一部分为不同烟雾吸入时间组,观察各组烟雾吸入48 h 的生存率;第二部分是选取烟雾吸入30 min 为致伤因素,对烟雾吸入后1,6,24 h 的血气分析?肺损伤病理评分?肺泡灌洗液?外周血白细胞?主要炎症因子?信号通路中主要信号因子?肝肾功能的变化进行检测?结果 (1)不同烟雾吸入时间组生存率结果为:84. 21% (15 min 组);25% (30 min 组),0(50 min 组); (2)烟雾吸入30 min 后1 h 碳氧血红蛋白?二氧化碳分压?乳酸值在烟雾吸入后1 h 内显著升高( P < 0. 05),此后可逐渐恢复到正常水平;与对照组相比,烟雾吸入后1,6,24 h 肺损伤评分(LIS)?肺泡灌洗液(BALF)中蛋白含量显著增高;BALF 中白细胞总数于烟雾吸入后显著升高,其中肺泡巨噬细胞比例呈现先降低后升高而中性粒细胞先升高后降低的趋势?对多种炎症因子及信号通路的研究发现,烟雾吸入1 h 内即可出现多种信号因子的活化,WB 及免疫荧光显示6 h 活化最显著,24 h 逐渐降低?烟雾吸入后的肝肾功能无特异性改变?结论 建立了一种稳定可靠且高致死率的模拟舰船火灾烟雾吸入肺损伤模型,烟雾吸入急性期存在多条炎症通路的广泛激活,伴有典型的炎性细胞改变及肺部损伤特点,可为此后的深入研究奠定基础?
英文摘要:
      Objective To develop a rat model of battleship fire?related smoke inhalation?induced acute lung injury using combustion of composite materials with a controllable temperature. Methods We designed a smoke?generating chamber and a test chamber. Sober rats were restricted to cages located inside the chamber during the experiments. In aim one, we investigated the survival rates at different inhalation times (15, 30, and 50 min). In aim two, we evaluated blood gas values, lung pathological scores, pro?inflammatory molecules, and protein concentrations in the bronchoalveolar lavage fluid, circulating white cells, and liver and renal functions at 1 h, 6 h, and 24 h after 30 min smoke inhalation. Results The survival rates at the different inhalation periods were 84. 21% (15 min), 25% (30 min), and 0% (50 min). There was a significant increase in carboxyhaemoglobin (COHB), lactate, and partial pressure of carbon dioxide (PCO2 ) at 1 h post injury ( P < 0. 05), which then gradually returned to normal. In the bronchoalveolar lavage fluid (BALF), the protein concentration and lung injury were score increased immediately after smoke inhalation, and persisted until 24 h. In the BALF, the total number of leukocytes cells significantly increased after smoke inhalation, while the proportion of macrophages significantly decreased at 6 h, then slightly recovered at 24 h; neutrophils showed the opposite trend. By western blot, there was a significant increase in signal pathway factors and inflammatory factors at 6 h recovery. There were no changes in the liver or renal functions after smoke inhalation. Conclusions This stable and reliable rat smoke inhalation injury model induced using our novel smoke generators is characterized by activation of inflammatory signaling pathways, inflammatory cell changes, and lung injury. This model may be useful for studies examining acute and chronic lung injury.
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