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目的研究大鼠体外循环(cardiopulmonary bypass,CPB)后肺脏损伤及其相关机制。方法 24只雄性SD大鼠随机均分成两组:伪手术组(Sham组)和体外循环组(CPB组),Sham组建立CPB模型管道,不进行体外循环;CPB组建立体外循环后流量逐步调至最大[≥100 ml/(kg·min)]维持转流60 min。于转流开始前(T0)和转流结束后(T1)、术后1 h(T2)、术后2 h(T3)、术后12 h(T4)行血清肿瘤坏死因子(tumor necrosis factor-α,TNF-α)、基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)因子检测及动脉血气分析。术后12 h(T4)获取支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF)和肺组织检测TNF-α、MMP-9浓度及肺组织和和核转录因子NF-κB(nuclear transcription factor-Kappa B,NF-κB)的表达水平,并行组织学检查。结果 CPB组CPB后大鼠血清、肺组织及BALF中炎症因子TNF-α、MMP-9均较Sham组明显上升,CPB组肺组织NF-κB蛋白表达水平显著高于Sham组(P<0.05);组织学检查发现CPB组表现为中性粒细胞浸润、肺间质水肿、出血、透明膜形成和坏死等病理变化。结论 CPB可导致肺组织NF-κB激活,上调TNF-α、MMP-9等炎症因子表达,引起肺损伤。
Objective To study the lung injury and its related mechanism after cardiopulmonary bypass (CPB) in rats. Methods Twenty-four male Sprague-Dawley rats were randomly divided into two groups: sham operation group (Sham group) and CPB group (Sham group). The CPB model was established in Sham group without cardiopulmonary bypass. CPB group was established after cardiopulmonary bypass To the maximum [≥ 100 ml / (kg · min)] to maintain the flow of 60 min. The serum levels of tumor necrosis factor-alpha (TNF-α) were measured before T0 and after T1, at 1 h after operation (T2), 2 h after operation (T3) and 12 h after operation (T4) α, TNF-α), matrix metalloproteinase-9 (MMP-9) and arterial blood gas analysis. The concentration of TNF-α and MMP-9 in bronchoalveolar lavage fluid (BALF) and lung tissue were measured at 12 h after operation (T4) and the expression of NF-κB and nuclear transcription factor-Kappa B , NF-κB) expression levels, parallel histological examination. Results Compared with Sham group, the levels of TNF-α and MMP-9 in serum, lung tissue and BALF of CPB group were significantly increased after CPB, while the expression of NF-κB in lung tissue of CPB group was significantly higher than that of Sham group (P <0.05) Histological examination showed that CPB group showed neutrophil infiltration, interstitial edema, hemorrhage, hyaline membrane formation and necrosis and other pathological changes. Conclusion CPB can induce the activation of NF-κB in lung tissue, up-regulate the expression of TNF-α, MMP-9 and other inflammatory cytokines and cause lung injury.