摘要目的 研究肢体缺血预处理对兔肺组织缺血再灌注后氧自由基及细胞因子分泌的影响.方法 将18只日本大耳白兔随机分为对照组(C组)、缺血再灌注组(I/R组)及肢体缺血预处理组(L组),每组6只.实验结束时,取肺组织测定湿/干重比(W/D)、超氧化物歧化酶(SOD)和髓过氧化物酶(MPO)活性、丙二醛(MDA)和肿瘤坏死因子(TNF)-α、白介素(IL)-6、IL-8及IL-10的含量;检测支气管肺泡灌洗液和血清中蛋白含量,计算肺通透性指数;观察肺组织病理学变化.结果 与I/R组比较,L组W/D、肺通透性指数、MPO活性、MDA和TNF-α、IL-6、IL-8的含量均降低(P<0.05),SOD活性(P<0.05)和IL-10含量升高(P<0.01).C、L两组间上述指标的差异无统计学意义(P>0.05).光镜榆查结果发现L组肺组织病理学改变较I/R组明显减轻.结论 肢体缺血预处理可以抑制缺血再灌注肺组织中氧自由基产生和促炎细胞因子TNF-α、IL-6、IL-8的释放,上调抗炎细胞因子IL-10的合成,从而减轻肺缺血再灌注损伤.

abstractsObjective To study the effects of limb ischemia preconditioning on pulmonary free radicals and cytokine levels during lung ischemia-reperfusion injury in rabbits. Methods Eighteen healthy rabbits were randomly divided into three groups: control group ( group C, n = 6), ischemia/reperfusion group (group I/R, n = 6) , limb ischemia preconditioning group ( group L, n = 6) . At the end of experiments, the wet to dry-weight ratio (W/D), activities of superoxide dismutase ( SOD) and myleoperoxidase (MPO) , levels of malondialdehyde ( MDA) and the contents of cytokines (TNF-α,IL-6, IL-8 and IL-10) were determined in lung tissues. Protein levels of bronchoalveolar lavage fluid and serum were measured to calculate the lung permeability index. Pathologic changes of lung tissues were also observed. Results Compared to the group I/R, the lung tissue W/D ratio, MPO activity, lung permeability index, MDA and the cytokines (TNF-α, IL-6 and IL-8) levels were significantly decreased in group L (P < 0. 05), while the SOD activity ( P < 0.05) and IL-10 contents were significantly increased (P < 0. 01). There was no statistical difference in the changes of the above parameters between group L and group C ( P > 0. 05). The morphologic damages were significantly reduced in group L than that in group I/R. Conclusion Limb ischemia preconditioning has protective effect against lung ischemia-reperfusion injury, which may at least in part through inhibiting the release of oxygen-derived free radicals and pro-inflammatory cytokines (TNF-α,IL-6,IL-8) and increasing the production of anti-inflammatory cytokine IL-10.