海水吸入致大鼠急性肺损伤模型的建立
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全军医药卫生“十五”科研项目(01MA145);上海市科委重点基础项目(03JC14002).


An acute lung injury model caused by seawater aspiration in rats
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    摘要:

    目的:建立海水吸入肺损伤动物模型.方法:24只大鼠随机分为对照组9只和模型组15只.模型组大鼠屏气9~10 s后吸入海水,4 ml/kg,分2次进行;对照组大鼠不吸入海水.于海水吸入前、海水吸入后10、30、60、120、240 min观察动脉血气和呼吸频率的变化,并记录动物的生存时间.4 h后处死动物,观察肺系数、支气管肺泡灌洗液(BALF)中总蛋白(TP)含量和白细胞计数以及肺组织形态学的变化.结果:与对照组相比,模型组大鼠吸入海水后呼吸频率显著增加,动脉血氧分压(PaO2)显著降低(P<0.05),之后虽逐渐回升,但一直维持在较低的水平;肺系数和TP含量均显著升高(P<0.05);白细胞计数显著增加(P<0.05);肺组织形态学显示明显的肺水肿、肺泡萎陷和炎细胞浸润情况.结论:成功建立海水吸入肺损伤的动物模型.

    Abstract:

    Objective: To establish an acute lung injury model by seawater aspiration in rats. Methods: Twenty-four rats were randomly allocated into 2 groups: control group (n= 9) and model group (n= 15). The acute lung injury model was established in rats by aspirating 2 ml seawater/kg body weight after 9-10 seconds of breath occlusion. The aspiration was repeated by the same means 2 rain later. Rats in control group aspirated no seawater. Arterial blood gases and respiratory rates were observed before aspiration and 10 min, 30 rain, 1 h, 2 h and 4 h after aspiration. The survival times of animal were also recorded. The rats were sacrificed 4 h after aspiration; the lung index, total protein (TP) contents, white blood cell (WBC) count in bronchoalveolar lavage fluid (BALF), and the pulmonary histopathology were observed. Results: Compared with control group, model group had a significantly increased respiratory rate and a decreased PaO2 (P〈0.05),which subsequently rose again and remained at a lower level. The model group also had a markedly increased lung index, TP contents and WBC counts (P〈 0.05). Obvious edema, alveolar atrophy and inflammatory infiltration were found in model rats. Conclusion: An acute lung injury model by seawater aspiration has been successfuly established

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  • 收稿日期:2006-01-04
  • 最后修改日期:2006-04-26
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  • 在线发布日期: 2006-06-20
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