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

发布时间：2018-06-17 11:46

本文选题：右美托咪定 + 胸部损伤　；参考：《基因组学与应用生物学》2017年03期

【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(p0.05),OI降低(p0.05),THSR组PaCO_2升高(p0.05),THSR组和治疗组的PaO_2、PaCO_2和OI差异具有统计学意义(p0.05);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(p0.05);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(p0.05),治疗组大鼠肺组织中TLR4和p-p38MAPK表达水平较THSR组显著下调(p0.05)。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。
[Abstract]:To investigate the effects of dexmetidine posttreatment on chest impact hemorrhagic shock and acute lung injury induced by resuscitation. In this study, 45 SPF male healthy rats were randomly divided into three groups. THSR group (chest impact-hemorrhagic shock / resuscitation group) and treatment group (dexmetomidine post-treatment group) were used to prepare acute lung injury models induced by chest impact-hemorrhagic shock / resuscitation. In the treatment group, 10 渭 g / kg dexmetomidine was injected intravenously after the establishment of the model. The blood was collected 6 hours after the model was made and the rats were killed. The blood gas analysis indexes of three groups were compared: PaO2 / Paco _ 2, oxygenation index (Oi), lung histopathology, inflammatory factor level (plasma IL-6 and IL-1 尾, protein concentration and white blood cell count in alveolar lavage fluid (BALFF), and expression of TLR4 and p-p38 MAPK in lung tissue. Compared with the normal saline group, the increase of Pao _ 2 in THSR group and the treatment group decreased the Paco _ 2 elevation of Paco _ 2 in THSR group, and the difference of PaO2Paco _ 2 and OI in THSR group and treatment group. There were significant differences between the two groups in lung histopathological injury score, plasma inflammatory factor BLAF protein and Pao _ 2 Paco _ 2 and OI in THSR group. The expression of TLR4 and p-p38 MAPK in lung tissue of rats in saline group and treatment group was higher than that in saline group, and the expression of TLR4 and p-p38 MAPK in lung tissue of treatment group was lower than that of THSR group. The expression of TLR4 and p-p38 MAPK in lung tissue of treatment group was significantly lower than that of THSR group. The posttreatment of dexmetidine could significantly reduce the acute lung injury induced by chest impact-hemorrhagic shock and resuscitation. The mechanism may be related to the inhibition of activation of TLR4 / p-p38 MAPK signaling pathway and the reduction of inflammatory response.
【作者单位】：三峡大学仁和医院重症监护室;
【分类号】：R459.7

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