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目的探讨七氟醚后处理对犬体外循环肺缺血/再灌注损伤的效果及晚期糖基化终末产物受体(receptor for ad-vanced glycosylation end products,RAGE)在此过程中的作用。方法 12只健康犬依据主动脉开放后是否吸入七氟醚随机分为两组:对照组(control,n=6)在主动脉开放后常规机械通气和实验组(test,n=6)在主动脉开放后吸入1MAC七氟醚,持续10min。在开胸后即刻(T1)、主动脉开放90min实验结束前(T2)留取肺组织标本和肺静脉血标本。标检测肺组织湿干重比(wet/dry weight,W/D);比色法检测肺组织髓过氧化物酶活性(myeloperoxidase activity,MPO);光镜观察并盲法评分比较肺组织病理学变化;分别采取RT-PCR方法、Western blot检测肺组织RAGE的表达;酶联免疫吸附法检测血清白介素6(IL-6)和肿瘤坏死因子α(TNF-α)含量。结果两组相比,实验组肺组织W/D、MPO、肺损伤评分、RAGE基因表达和蛋白表达、IL-6和TNF-α含量在T2时较对照组降低(P<0.05);组内比较,所有指标实验结束时均较基础值明显升高(P<0.05)。结论七氟醚后处理对体外循环缺血/再灌注导致的肺损伤具有一定的保护作用,可能与其抑制RAGE合成与激活有关。
Objective To investigate the effect of sevoflurane postconditioning on lung ischemia / reperfusion injury during cardiopulmonary bypass and the role of receptor for ad-vanced glycosylation end products (RAGE) in this process. Methods Twelve healthy dogs were randomly divided into two groups according to whether or not sevoflurane was inhaled after aortic opening: control (n = 6), routine mechanical ventilation and experimental group (test, n = 6) After inhalation of arterial 1 MAC sevoflurane, lasted 10min. Immediately after thoracotomy (T1), aortic opening 90min before the end of the experiment (T2) to take lung tissue samples and pulmonary venous blood samples. The wet / dry weight (W / D) of the lung tissue was measured and the myeloperoxidase activity (MPO) was measured by colorimetric method. The lung histopathology The expression of RAGE in lung tissue was detected by RT-PCR and Western blot respectively. The levels of serum interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected by enzyme-linked immunosorbent assay. Results Compared with the control group, the W / D, MPO, lung injury score, RAGE gene expression and protein expression, IL-6 and TNF-αlevels in the experimental group were significantly decreased at T2 (P <0.05) Compared with the baseline, all indexes were significantly increased at the end of the experiment (P <0.05). Conclusion Sevoflurane postconditioning may have a protective effect on lung injury induced by cardiopulmonary bypass / reperfusion, which may be related to the inhibition of RAGE synthesis and activation.