不同潮气量机械通气诱发的肺损伤大鼠肺组织中CXCR2表达  

Effects of different volume mechanical ventilation on the levels of CXCR2 protein in lung of rats

作　　者：宋秀梅[1] 王月兰[1] 刘洋[1] 

机构地区：[1]山东省千佛山医院麻醉科,济南市250014

出　　处：《临床麻醉学杂志》2012年第9期905-907,共3页Journal of Clinical Anesthesiology

基　　金：山东省医药卫生计划项目(2007HZ081)

摘　　要：目的探讨不同潮气量机械通气大鼠肺组织中巨噬细胞炎性蛋白2(MIP-2)及CXCR2蛋白的表达。方法清洁级Wistar大鼠30只,雄雌不拘,体重200～250g,随机均分为三组。实验前12h禁食,自由饮水。对照组,仅作气管切开插管,不行机械通气;小潮气量组潮气量VT7ml/kg,大潮气量组VT40ml/kg,两组气管切开插管后接小动物呼吸机控制呼吸,调节RR40次/分,吸呼比1∶2,空气吸入,通气4h,建立机械通气诱发肺损伤大鼠动物模型。对照组在气管插管后即刻,余两组在机械通气结束后,立即剖胸,取大鼠肺组织,收集支气管肺泡灌洗液(BALF)。RT-PCR法测定肺组织中CXCR2的mRNA表达、免疫组化测定肺组织CXCR2的蛋白表达和HE染色观察肺组织病理学变化,ELISA法测定肺组织匀浆中MIP-2蛋白水平,测定BALF中PMN计数。结果与对照组和小潮气量组比较,大潮气量组MIP-2蛋白及其受体CXCR2蛋白和mRNA表达增加(P<0.05),灌洗液中PMN计数增加(P<0.05),肺炎症反应明显加重;与对照组比较,小潮气量组上述指标无明显变化。结论大潮气量机械通气引起肺组织中炎症因子MIP-2及其受体CXCR2表达增加,肺组织炎症反应明显,损伤加重,是机械通气相关肺损伤的发生机制之一。Objective To investigate the effects of different volume mechanical ventilation on the levels of CXCR2 and MIP-2 in the lung of rats. Methods Thirty normal Wistar rats weighing 200- 250 g were randomly divided into 3 groups （n = 10 each）. Control group the animals were tracheotomized, spontaneously breathing; The other two groups mechanically ventilated with respiratory rate（RR） 40 bpm, FiO2 21%, Time （I ： E） 1 ： 2, ventilation time （t） 4 h, small volume group： tidal volume V_T 7 ml/kg; large volume group： V_T 40 ml/kg. After ventilation, the rats were sacrificed and the lungs were removed for microscopic examination. The levels of CXCR2 mRNA in the lung were detected by RT-PCR and the protein were detected by immunochemistry. The expression of MIP-2 in the lung was detected by ELISA and PMN in broncho-alveolar lavage fluid （BALF） were counted. Results The expression of CXCR2 protein and mRNA, MIP-2 protein in lung, and PMN count in BALF were elevated more significantly in large volume group compared with that in control group and small volume group （P 〈 0.05）, and the inflammation in lung was more seriously in large volume group. But the difference between control group and small volume group was not significant. Conclusion Mechanical ventilation with large tidal volume increases production of CXCR2 and MIP-2 in lung tissues and induced lung injury.

关 键 词：呼吸 人工 肺损伤 CXCR2 

分 类 号：R614[医药卫生—麻醉学]