胸部开放伤海水浸泡致急性肺损伤的实验研究

来源 :中国危重病急救医学 | 被引量 : 0次 | 上传用户:ringogogo
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目的 :探讨胸部开放伤海水浸泡致急性肺损伤的特点 ,为研究救治方案提供依据。方法 :实验动物致伤后随机分为对照组 (10只 )、海水浸泡组 (10只 )和生理盐水浸泡组 (5只 )。对照组为单纯胸外伤 ,后 2组动物于致伤后分别置入人工配制的海水或生理盐水中 ,于伤前及入水后 0 .5、1、2、3和 4小时取血测定肿瘤坏死因子α(TNFα)和白介素 1β(IL 1β)变化 ,同时监测血流动力学、呼吸系统和动脉血气变化。动物活杀或死后立即取肺标本行光镜和电镜检查。对照组除不浸泡海水 (或生理盐水 )外其它处理同海水浸泡组。结果 :海水浸泡组动物死亡率明显高于对照组和生理盐水浸泡组 ,且生存时间明显短于后 2组 ,平均生存时间为 45分钟。海水浸泡组的急性肺损伤明显重于对照组和生理盐水浸泡组 ,表现为严重的低氧血症和高碳酸血症、肺含水量明显增加、血浆 TNFα和 IL 1β伤后明显升高并且高峰时间明显提前。结论 :海水浸泡加剧胸外伤致急性肺损伤的程度 ,导致呼吸及循环系统进行性衰竭 ,加速实验动物死亡 Objective: To investigate the characteristics of acute lung injury caused by seawater immersion in chest open wounds, and to provide basis for researching the treatment plan. Methods: Experimental animals were randomly divided into control group (10 rats), seawater immersion group (10 rats) and saline immersion group (5 rats). The control group was simple thoracic trauma. The animals in the latter two groups were implanted into artificial seawater or saline respectively after injury. Tumor necrosis was measured at 0.5, 1, 2, 3 and 4 hours after injury Factors α (TNFα) and interleukin 1β (IL 1β) changes, while monitoring hemodynamic, respiratory and arterial blood gas changes. Immediately after the animal killed or died, the lungs were examined by light microscope and electron microscope. In addition to the control group is not immersed in seawater (or saline) other treatment with seawater immersion group. Results: The mortality of seawater immersion group was significantly higher than that of the control group and saline immersion group, and the survival time was significantly shorter than the latter two groups, with an average survival time of 45 minutes. Acute lung injury in seawater immersion group was significantly higher than that in control group and saline immersion group, showing severe hypoxemia and hypercapnia, lung water content increased significantly, plasma TNFα and IL 1β significantly increased after injury and the peak Obviously ahead of time Conclusion: Seawater immersion exacerbated the degree of acute lung injury caused by thoracic injury, leading to progressive failure of respiratory and circulatory system and accelerated death of experimental animals
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