高渗盐水对创伤失血性休克兔促炎与抗炎细胞因子和黏附分子表达的影响及其意义  

Effects of hypertonic saline on proinflammatory and antiinflammatory cytokines and adhesion molecule expressions in rabbits with traumatic hemorrhagic shock

作　　者：郑国寿[1] 白祥军[1] 占成业[2] 邓普珍[2] 

机构地区：[1]华中科技大学同济医学院附属同济医院,湖北武汉430030 [2]华中科技大学同济医学院附属同济医院急诊科,湖北武汉430030

出　　处：《中国急救医学》2005年第7期498-500,共3页Chinese Journal of Critical Care Medicine

摘　　要：目的研究高渗盐水(HS)对创伤失血性休克时促炎与抗炎细胞因子和黏附分子表达的影响及其在急性肺损伤(ALI)防治中的作用。方法新西兰白兔30只随机分为3组:假手术组(Sham组)、生理盐水处理组(NS组)、高渗盐水治疗组(HS组)。双抗体夹心ELISA法测定休克前、休克末及复苏后2、4h血清肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-6、IL-10及可溶性细胞间黏附分子-1(sICAM-1)的浓度;逆转录-聚合酶链反应(RT-PCR)检测肺组织各细胞因子及细胞间黏附分子-1(ICAM-1)和mRNA表达水平;显微镜观察肺组织的病理改变。结果与NS组比较,HS组复苏后4hTNF-α、IL-6、ICAM-1血清浓度及肺组织表达水平均有不同程度下降,而IL-10的浓度及mRNA水平明显增高(P<0·05,P<0·01),肺组织的病理学损伤显著减轻。结论HS治疗可抑制创伤失血性休克时促炎细胞因子及黏附分子的合成、分泌或表达,同时增加抗炎细胞因子的释放与表达,减轻肺部的炎症反应,发挥对肺损伤的保护作用。Objective To investigate the effects of hypertonic saline on expressions of cytokines and adhesion molecule and prevention and treatment of acute lung injury(ALI).Methods 30 rabbits were randomly divided into three groups:control group(Sham group),normal saline group(NS group),and hypertonic saline group(HS group).Traumatic hemorrhagic shock model of the rabbits were established and followed by resuscitation with NS or HS(75 g/L sodium chloride,4 mL/kg).Serum concentrations of tumor necrosis factor-α(TNFα),interleukin-6(IL-6),interleukin-10(IL-10)and soluble intercellular adhesion molecule-1(sICAM-1)were determined by sandwich enzyme-linked immuno sorbent assay(ELISA) in pre-shock,post-shock,2 h and 4 h after fluid resuscitation.The mRNA levels of cytokines and ICAM-1 in pulmonary tissues were measured with reversal transcription-polymerase chain reaction(RT-PCR).Pathologic changes of pulmonary tissues were observed under microscope.Results Compared with NS group, serum concentrations and mRNA levels of TNFα,IL-6 and ICAM-1 reduced in different degrees,whereas the release and expression of IL-10 markedly increased(P<0.05,P<0.01),and pathologic changes of pulmonary tissues significantly attenuated in 4 h after fluid resuscitation in HS group.Conclusion HS can protect traumatic hemorrhagic shock induced lung injury by inhibiting the synthesis,secretion and expression of proinflammatory cytokines and adhesion molecule,upregulating the release and expression of antiinflammatory cytokines,and relieving pulmonary inflammation.

关 键 词：高渗盐水 创伤失血性休克 细胞因子 促炎 抗炎 黏附分子 急性肺损伤 

分 类 号：R641[医药卫生—外科学]