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胸部开放伤后海水浸泡对实验犬前炎症细胞因子的影响 被引量:7

Effect of open chest injury and seawater immersion on interleukin-1β and tumor necrosis factor-α level
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摘要 目的 探讨海水浸泡胸部开放伤对实验犬血浆前炎症细胞因子肿瘤坏死因子 α(TNF α)和白细胞介素 1β(IL 1β)水平变化的影响。 方法 实验动物致伤后随机分为对照组 (n =10 )、海水浸泡组 (n =10 )和生理盐水浸泡组 (n =5 )。对照组为单纯胸外伤 ,海水浸泡组和生理盐水浸泡组的动物于致伤后分别置入人工配制的海水或生理盐水中 ,于伤前及浸泡后15、30、45min及 1、2、3和 4h取血测定TNF α和IL β变化 ,同时监测血流动力学、呼吸系统和动脉血气变化。对照组除不浸泡海水外处理同海水浸泡组。结果 海水浸泡组的血TNF α和IL 1β伤后明显升高并且高峰出现时间明显提前。急性肺损伤明显重于对照组和生理盐水浸泡组。结论 胸外伤后海水浸泡可能启动了全身前炎症细胞因子TNF α和IL 1β的过度表达 ,并且这种变化可能在急性肺损伤的发病机理中起重要作用。 Objective To evaluate the effect of open chest injury and seawater immersion on interleukin-1β(1L-β)and tumor necrosis factor-α(TNF-α)level.Methods Twenty-five health dogs were divided into three groups.A model of right open pneumothorax was established.Control group(n=10) was simple chest injury.Seawater immersion group(n=10)had seawater immersion after open chest injury and normal saline solution group(n=5)was immersed into normal saline solution after the injury.after induction of chest trauma animals in seawater immersion group were immersed in artificial seawater.Blood samples were taken at eight different time intervals for assessing blood gas,plasma level of TNF-α and IL-1β.The hemodynamic and respiratory changes were recorded.At the end of study lung was harvested for assessing lung water content and ratio of wet weight and dry weight.Results The plasma levels of TNF-α and IL-1β significantly increased at 30 minutes and reached the highest level at 60 minutes after seawater immersion.The time of peak level appeared earlier in seawater immersion group than that in control group and normal saline immersion group.Conclusion Seawater immersion after open chest injury could result in excessive expression of TNF-α and IL-1β and these changes may play an important role in the pathogenesis of acute lung injury.
出处 《中国急救医学》 CAS CSCD 北大核心 2001年第6期314-316,共3页 Chinese Journal of Critical Care Medicine
基金 解放军总后勤部卫生部"九五"指令性课题 ( 96 L0 0 4)
关键词 海水浸泡 开放性胸部伤 前炎症细胞因子 肿瘤坏死因子 白细胞介素-1Β Seawater immersion Open chest injury Pro-inflammatory mediator Interleukin-1β Tumor necrosis factor-α
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