失血性休克再灌注后肺组织的炎症病理机制的研究  

A study on mechanism or inflammatory pathology in the lung tissues ischemia - reperfusion injury following hemorrhagic shock

作　　者：尹文[1] 虎晓岷[1] 李云龙 支少敏[1] 袁静[3] 张金山[1] 黄杨[1] 

机构地区：[1]中国人民解放军第四军医大学西京医院急诊科,陕西西安710032 [2]陕西扶风县人民医院 [3]中国人民解放军第五医院

出　　处：《中国急救医学》2003年第11期756-758,共3页Chinese Journal of Critical Care Medicine

基　　金：国家自然科学基金资助项目(No.30000165)

摘　　要：目的 探讨失血性休克缺血/再灌注(I/R)损伤后肺组织炎症反应的分子病理机制。方法 采用失血性休克I/R家兔模型,进行动脉血气、肺湿/干(W/D)比值和支气管肺泡灌洗液(BALF)中肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)以及C3a、C5a、白蛋白含量和中性粒细胞数量的测定,并进行肺组织病理学光镜检查。用原位杂交、免疫组织化学结合图象分析检测肺组织IKK-β mRNA表达、NF-kB活性的变化。结果 模型组肺组织IKK-β mRNA表达、NF-kB活性和BALF中上述各项检测指标均有不同程度的升高,肺组织明显炎症病理改变。结论 NF-kB信号通路激活诱发的细胞因子和炎性介质释放可能是I/R过程中脏器损伤的重要病理机制。Objective To investigate the possible molecular pathogenesis of inflammatory reaction in the lung tissues ischemia - reperfusion(I/R)injury following hemorrhagic shock. Methods Rabbit model of ischemia - reperfusion injury following hemorrhagic shock was used in this study. The blood air lung wet/dry(W/D) weight and contents of the tumor necrosis factor - α(TNF - α), interleukin - 6 (IL - 6), the neutrophils cell counts, albumin, C3a, C5a in bronchoalveolar lavage fluid (BALF)were analyzed. The pathological changes were examined with light microscope in lung tissues. The expressions of IKK - β and activation of NF - κB in the lung tissues were measured by in situ hybridization, immunohitochemistry combined with in situ quantitative analysis, respectively. Results In ischemia - reperfusion injury group, the expression of IKK - β mRNA, activation of NF - κB in lung tissues and the levels of all inspection guideline in BALF were obviously higher than those of normal group, and the severity of lung tissue damages increased in ischemia - reperfusion(I/R)injury following hemorrhagic shock. Conclusion Release of inflammatory cytokines induced by NF - κB signal transduction pathways might be an important pathogenesis in the lung tissue ischemia - reperfusion(I/R)injury following hemorrhagic shock.

关 键 词：失血性休克 肺 缺血/再灌注 核因子-ΚB 信号转导 

分 类 号：R363.2[医药卫生—病理学]