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目的探讨缺血后适应对肢体缺血再灌注后肺损伤的影响及作用机制。方法将实验动物随机分为三组:对照组、缺血再灌注组(IR)和缺血后适应组(IPC)。检测各组血清及肺组织中丙二醛(MDA)及超氧化物岐化酶(SOD)的含量变化,并检测肺组织中髓过氧化物酶(MPO)的活性。HE染色光镜下观察肺组织病理形态学改变。结果与对照组比较,IR组和IPC组动物血清MDA含量均明显升高(P<0.01),而SOD含量则明显降低(P<0.01)。与IR组比较,IPC组血清MDA含量明显下降(P<0.01),SOD含量明显升高(P<0.01)。与对照组比较,IR组和IPC组动物肺组织中MDA含量均明显升高(P<0.01),而SOD含量则明显降低(P<0.01);IPC组与IR组之间比较,IPC组肺组织中MDA含量较IR组明显下降(P<0.01),而SOD含量较IR组明显升高(P<0.01)。IR组动物肺组织中MPO活性明显高于对照组和IPC组(P<0.01),IPC组肺组织中MPO活性略高于对照组,但差异无统计学意义。光镜下IR组表现为肺间质水肿和中度炎症等肺损伤病理改变,而IPC组肺损伤病理改变较轻。结论 IPC可减轻大鼠LIR后的肺损伤,其机制与抑制氧化应激、PMN的活化及炎症反应的扩散有关。
Objective To investigate the effect of post-ischemic postconditioning on lung injury after limb ischemia-reperfusion and its mechanism. Methods The experimental animals were randomly divided into three groups: control group, ischemia reperfusion group (IR) and ischemic postconditioning group (IPC). The content of malondialdehyde (MDA) and superoxide dismutase (SOD) in serum and lung tissue of each group were detected, and the activity of myeloperoxidase (MPO) in lung tissue was detected. The pathological changes of lung tissue were observed under HE staining. Results Compared with the control group, serum MDA levels in both IR and IPC groups were significantly increased (P <0.01), while SOD levels were significantly decreased (P <0.01). Compared with IR group, the content of MDA in serum of IPC group decreased significantly (P <0.01), and the content of SOD increased significantly (P <0.01). Compared with the control group, the content of MDA in lung tissue of IR group and IPC group were significantly increased (P <0.01), while the content of SOD was significantly decreased (P <0.01); IPC group and IR group Compared with IR group, the content of MDA decreased significantly (P <0.01), while the content of SOD increased significantly (P <0.01). The MPO activity in lung tissue of IR group was significantly higher than that of control group and IPC group (P <0.01). The activity of MPO in lung tissue of IPC group was slightly higher than that of control group, but the difference was not statistically significant. Under light microscope IR group showed lung interstitial edema and moderate inflammation and other pathological changes of lung injury, and lung injury in IPC group lighter pathological changes. Conclusion IPC can reduce lung injury after LIR in rats, and its mechanism is related to inhibition of oxidative stress, activation of PMN and the proliferation of inflammatory reaction.