摘要
为探讨右美托咪定后处理对胸部撞击失血性休克和复苏致急性肺损伤的影响。本研究选取45只SPF级雄性健康大鼠依据随机数字表法将其分为3组,生理盐水组、THSR组(胸部撞击-失血性休克/复苏组)和治疗组(右美托咪定后处理组),THSR组和治疗组制备胸部撞击-失血性休克/复苏致急性肺损伤模型,治疗组模型建立后静脉注射右美托咪定10μg/kg。模型制备6 h后采血,并处死大鼠。比较3组大鼠血气分析指标(PaO_2,PaCO_2和氧合指数(OI))、肺组织病理形态、炎症因子水平(血浆IL-6和IL-1β水平,肺泡灌洗液(BALF)中蛋白浓度和白细胞数目)以及肺组织中TLR4和p-p38MAPK表达水平。与生理盐水组比较,THSR组和治疗组的PaO_2升高(p<0.05),OI降低(p<0.05),THSR组PaCO_2升高(p<0.05),THSR组和治疗组的PaO_2、PaCO_2和OI差异具有统计学意义(p<0.05);THSR组疗组大鼠肺组织病理学损伤评分、血浆炎症因子(BLAF蛋白,白细胞计数,IL-6和IL-1β)水平最高,治疗组次之,生理盐水组最低(p<0.05);THSR组和治疗组大鼠肺组织中TLR4和p-p38MAPK表达较生理盐水组上调(p<0.05),治疗组大鼠肺组织中TLR4和p-p38MAPK表达水平较THSR组显著下调(p<0.05)。右美托咪定后处理可明显减轻胸部撞击-失血性休克和复苏致急性肺损伤,其起效机制可能与抑制TLR4/p-p38MAPK信号通路激活,降低机体炎性反应有关。
To explore the influence of dexmedetomidine on acute lung injury induced by thoracic trauma-hemorrhagic shock and resuscitation, 45 healthy adult male SPF rats were divided into three groups according to random number method： saline group, THSR group （thoracic trauma-hemorrhagic shock/resuscitation group） and treatment group （dexmedetomidine treatment group）. Both THSR and treatment groups were prepared rats model of acute induced by trauma-hemorrhagic shock/resuscitation, and treatment group was treated with intravenous dexmedetomidine 10 μg/kg after model establishment. Blood was withdrawn after the model was prepared for 6 h, and then rats were sacrificed. Compare the blood gas analysis indicators （PaO2, PaCO2 and oxyg-enation index （OI））, pathology morphology of lung tissue, levels of inflammatory cytokines （plasma IL-6 and IL-1β levels, protein concentration and the number of white blood cells in bronchoalveolar lavage fluid （BALF））,and the expression level of TLR4 and p-p38MAPK in lung tissue of three groups. Compared with saline group, PaO2 increased in THSR group and treatment group （p〈0.05）, OI decreased （p〈0.05）, PaCO2 increased in THSR group （p 〈0.05）, and difference of PaO2, PaCO2, OI between THSR group and treatment group was statistically significant （p〈0.05）. The level of lung tissue pathological lesion score and plasma inflammatory cytokines （BLAF protein, white blood cell count, IL-6 and IL-1 β） in THSR group was the highest, then was treatment group, and the lowest was saline group （p 〈0.05）. Compared with the saline group, the expression level of TLR4 and p-p38MAPK increased in THSR group and treatment group （p 〈0.05）, and that in the treatment group was significantly lower than THSR group （p 〈0.05）. The results showed that dexmedetomidine treatment could significantly mitigate acute lung injury induced by thoracic trauma-hemorrhagic shock and resuscitation in rats, which might be related to the inhibition of TLR4/p-p38M
出处
《基因组学与应用生物学》
CAS
CSCD
北大核心
2017年第3期1204-1209,共6页
Genomics and Applied Biology
关键词
右美托咪定
胸部损伤
休克
肺损伤
Dexmedetomidine, Chest injury, Shock, Lung injury
