单侧胸部撞击致家兔对侧肺生物学标志的变化  

Changes of biological variables in contralateral lung after unilateral blunt trauma of chest in rabbits

作　　者：何家庆[1] 蒋耀光[2] 王如文[2] 蹇华胜[1] 吴秋平[3] 

机构地区：[1]第三军医大学大坪医院野战外科研究所急救部,重庆400042 [2]第三军医大学大坪医院野战外科研究所胸心外科,重庆400042 [3]第三军医大学新桥医院胸外科

出　　处：《中华急诊医学杂志》2007年第2期163-166,共4页Chinese Journal of Emergency Medicine

基　　金：重庆市科委资助项目（7453）

摘　　要：目的研究单侧胸部撞击致家兔对侧肺损伤和早期炎症介质TNF-α在继发性肺损伤中的作用。方法选取新西兰大白兔48只，动物被随机分为正常对照组，伤后1、6、24h各组。采用BIM-Ⅱ型生物撞击机复制单侧胸部撞击伤动物模型。在伤后1、6、24h测定双肺生物学标志（肺湿／干重比、支气管肺泡灌洗液中性粒细胞、蛋白含量、肺微血管通透性）的变化，RT-PCR法测TNF-α mRNA在双侧肺组织中的表达。结果在伤后1、6、24h与正常对照组相比双肺生物学标志均出现明显的变化（P〈0．05或P〈0．01），TNF-α mRNA在双侧肺组织中表达增加。结论单侧胸部撞击伤后，对侧肺生物学标志的改变和肺组织的病理变化程度一致，与对侧肺的机械性损伤因素和继发性炎症反应有关；TNFα mRNA在肺组织中的表达增加，提示内源性炎症介质在继发性肺损伤的发生、发展过程中发挥重要作用。Objective To study effects of contralateral lung induced by unilateral blunt trauma and TNF-α on secondary lung injury in rabbits. Method Forty-eight New Zealand white rabbits were randomly divided into control group and groups at different time points after trauma （at 1 hours, 6 hours, and 24 hours, respectively）. The animal models of unilateral chest impact injury were induced by BIM-Ⅱ biological impact machine. The changes of biological variables, including lung wet/dry weight ratio, count of pol （PMN） and protein level in brenchoalveolar lavage fluid （BALF）, and pulmonary micrevessel permeability, were analyzed in bilateral lungs, and changed significantly the expression of TNF-α mRNA in the lung was determined with reverse transcription polymerase chain raction （RT-PCR） technique at 1, 6 hours, and 24 hours after unilateral chest blunt trauma. Results Pulmonary biological variables changed significantly in both lungs at different time points compared with control group （P 〈 0.05, or P 〈 0.01 ）. The expression of TNF-α mRNA increased in bilateral lungs after trauma. Conclusions The changes of biological variables in contralateml lung were in accordance with pathological changes of pulmonary tissue after unilateral chest impact injury, and were related to mechanical injury and secondary inflammatory reaction of eontralateml lung. Increasing of TNF-α mRNA expression in both lungs indicated that endogenous inflammatory mediator played an important role in development of secondary lung injury.

关 键 词：肺 生物学标志 对冲型肺损伤 胸部撞击伤 肿瘤坏死因子-Α 

分 类 号：R686[医药卫生—骨科学]