高张溶液复苏大鼠创伤失血性休克对肺组织I-κBα水平的影响  

Effect of resuscitation with hypertonic solution on Ⅰ-κBα in lung tissues following traumatic/hemorrhagic shock

作　　者：张良成[1] 王宏梗[2] 周琳瑛[3] 袁世荧[4] 曾邦雄[4] 

机构地区：[1]福建医科大学附属协和医院麻醉科,福建福州350001 [2]福建医科大学附属第二医院麻醉科,福建泉州362000 [3]福建医科大学电镜室,福建福州350004 [4]华中科技大学附属协和医院麻醉科,湖北武汉430022

出　　处：《中国药理学通报》2007年第1期102-105,共4页Chinese Pharmacological Bulletin

基　　金：福建省科技厅科研资助项目(No2003D03);福建省卫生厅"百千万人才"专项基金资助项目

摘　　要：目的探讨高张溶液复苏大鼠THS对肺组织I-κBα水平及该作用对减轻急性肺损伤的意义。方法实验大鼠分为假创伤失血性休克(Sham)组、大容量等张乳酸钠林格氏液+6%羟乙基淀粉液(RLH)复苏组和小容量高张(7·5%氯化钠)液+6%羟乙基淀粉溶液(HTH)复苏组。采用Westernblot技术检测肺组织I-κBα蛋白含量;以RT-PCR检测ICAM-1mRNA表达水平;以分光光度法测定肺组织MPO活性;光镜下评估肺炎症损伤程度;以干/湿重比代表肺组织水含量。结果与Sham组比较,肺组织I-κBα含量RLH组明显降低(P<0·01),HTH组轻微降低且明显高于RLH组(P<0·01);而ICAM-1mRNA表达水平RLH组明显增高,HTH组仅轻度增高,低于RLH组(P<0·05);RLH组MPO活性和炎症损伤评分也均明显高于HTH和Sham两组(P<0·01),HTH组与Sham组比较差异无统计学意义(P>0·05);肺水含量在RLH组也有所增高。结论HTH可明显抑制大鼠THS复苏后肺组织I-κBα的降低,此作用可能与其抑制THS后ICAM-1表达增高和中性粒细胞在肺部大量聚集、从而减轻急性肺损伤有关。Aim To determine the effect of hypertonic solutions resuscitating traumatic-hemorrhagic shock （THS） on Ⅰ-κBα content in lung tissu of rats. Methods 24 healthy male SD rats were divided into three groups： Sham, THS resuscitated with Ringer＇s lactate/ Hydroethylstarch solution （ RLH ）, THS resuscitated with 7. 5% Sodium chloride/Hydroethylstarch solution （HTH）. Western blotting was used to evaluate Ⅰ-κBα level. ICMA-1 mRNA expression was detected through RT-PCR technique. MPO activity and water content in lung tissue were defined with colormetric analysis and measurement of dry/wet ratio respectively. Morphological changes in lung under lightmicroscope were performed by two pathologists. Results 24 hours after HTS resuscitated with RLH, Ⅰ-κBα content decreased, and ICMA-1 mRNA expression in lung tissues and neutrophils lung sequetration as well as scores of acute lung injury increased obviously. Changes of these indices mentioned above were inhibited notably when rats were resuscitated with HTH. Conclusions These results suggest HTH resuscitation for HTS reduces the early acute lung injuries through its inhibition of Ⅰ-κBα degrading in lung tissues, which is directly linked to NF-κB activation. NF-κB activation is responsible for inflammatory genes, such as gene encoding for ICAM, transfer and expression.

关 键 词：休克/创伤失血性 高渗溶液 ICAM-1 Ⅰ-κBα 急性肺 损伤 

分 类 号：R-332[医药卫生] R322.35