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目的探讨七氟烷对大鼠缺血再灌注损伤肺组织的保护作用及其机制。方法 30只SD大鼠分为假手术组(Sham组)、缺血再灌注组(Ischemia reperfusion,I/R组)及七氟烷处理组(Ischemia reperfu-sion+sevoflurane;I/R+S组),每组10只。在全身麻醉下建立大鼠肺缺血再灌注损伤模型,Sham组:开胸游离左肺门后,未予阻断;I/R组:阻断左肺门45min而后松开血管夹形成缺血再灌注;I/R+S组:在实验过程中持续吸入七氟烷。再灌注后180min的Sham组、I/R组、I/R+S组的肺组织观察形态学变化,免疫组化法检测各组肺组织ICAM-1及NF-кB表达情况,检测光密度值(OD)。检测支气管肺泡灌洗液(Bronchoalveolar lavage fluid;BALF)中总蛋白含量、肺组织干/湿质量比(Dry/Wet;D/W)、肺组织髓过氧化物酶(Myeloperoxidase;MPO)及超氧化物歧化酶(Superoxide dismutase;SOD)含量。结果病理切片显示,I/R组肺泡和肺间质内白细胞聚集成团,肺泡结构破坏,间隔增宽,肺泡腔严重出血水肿,肺损伤较I/R+S组更加严重。I/R组、I/R+S组均随着再灌注时间的延长表现出明显的肺损伤变化,肺组织ICAM-1及NF-кB表达明显增加,OD值明显增高(P<0.05);肺组织BALF总蛋白和MPO含量明显升高、肺组织D/W和SOD显著降低(P<0.05);与C组、I/R组相比,I/R+S组各项观察指标在不同时间点均存在统计学差异。结论七氟烷降低缺血再灌注肺组织ICAM-1及NF-кB的表达,可减轻大鼠肺缺血再灌注损伤。
Objective To investigate the protective effect of sevoflurane on lung injury induced by ischemia-reperfusion in rats and its mechanism. Methods Thirty Sprague-Dawley rats were randomly divided into Sham group, Ischemia reperfusion group and Ischemia reperfu-sion + sevoflurane group ), 10 in each group. The model of lung ischemia-reperfusion injury in rats was established under general anesthesia. Sham group: without left thoracotomy, the left lung hilum was not blocked; I / R group: Reperfusion; I / R + S group: Continuous inhalation of sevoflurane during the experiment. The morphological changes of lung tissue were observed in Sham group, I / R group and I / R + S group at 180min after reperfusion. The expression of ICAM-1 and NF-κB in lung tissue of each group were detected by immunohistochemistry. The optical density (OD). The content of total protein in bronchoalveolar lavage fluid (BALF), the ratio of dry / wet D / W, Myeloperoxidase (MPO) and superoxide Superoxide dismutase (SOD) content. Results The pathological sections showed that alveolar and interstitial leukocytes aggregated into clusters in I / R group, the alveolar structure was destroyed, the interval was widened, the alveolar cavity was severely hemorrhaged and edematous. The lung injury was more serious than I / R + S group. The expression of ICAM-1 and NF-κB in lung tissue were significantly increased and the OD value was significantly increased in I / R group and I / R + S group with prolongation of reperfusion time (P <0.05). Compared with C group and I / R group, the observation indexes of I / R + S group were different in different groups There were statistical differences between the time points. Conclusion Sevoflurane can reduce the expression of ICAM-1 and NF-κB in lung tissue after ischemia-reperfusion in rats, and can reduce the lung ischemia-reperfusion injury in rats.