缺血后处理减轻肺缺血再灌注损伤的效果及机制探讨

Effect of ischemic postconditioning on alleviating lung ischemia-reperfusion injury in rats and its mechanism

目的观察缺血后处理减轻大鼠在体肺缺血再灌注损伤的效果,并探讨其机制。方法将24只健康SD大鼠随机分为假手术组(SO组)、缺血再灌注组(IR组)、缺血后处理组(IPC组),各8只。所有大鼠开胸后游离左侧肺门,用阻断带控制灌注时间。SO组持续灌注105 min;IR组(为对照)缺血45 min,再灌注60 min;IPC组缺血45 min、灌注1 min、缺血1 min,反复5次,然后全面恢复灌注50 min。处死大鼠取肺组织。行肺组织形态学检查,检测肺组织中丙二醛(MDA)、超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)水平,肺组织湿/干重比(W/D),结果光镜下观察IPC组肺泡中渗出物、红细胞和白细胞均少于IR组,肺间质中的多形核白细胞浸润亦较少。与IR组相比,IPC组肺组织中MDA、MPO水平及W/D下降,SOD升高(P均<0.05);与SO组相比,IPC组和IR组肺组织中MDA、MPO水平及W/D均升高,SOD均降低(P均<0.01)。结论缺血后处理可减轻大鼠肺缺血再灌注损伤,其机制与其抑制再灌注后氧自由基的过量生成有关。

Objective To observe the effect of ischemic postconditioning （IPC） on alleviating lung ischemia-reperfu- sion （IR） injury in rats and to explore its mechanism. Methods A total of 24 rats were randomly divided into 3 groups, 8 in each： Sham-operation group （SO group）, ischemia-reperfusion group（ IR group）, and ischemic postconditioning group （ IPC group）. In SO group, continuous infusion for 105 min; in IR group （ as control group）, 45 min of ischemia, reperfusion for 60 min; in IPC group, ischemia for 45 min, infusion for 1 min, then ischemia for 1 min, repeating 5 times, and after that full restoration of perfusion for 50 min. The rats were killed to obtain the lung tissue. Malondialdehyde （MDA）, superoxide dismutase （SOD）, myeloperoxidase （MPO） level, lung wet / dry weight ratio （W/D） were detected by lung histomorphological examination. Results In IPC group, the alveolar exudates, red blood cells and white blood cells were fewer than those in IR group, which were observed under light microscope; and the polymorphonuclear leukocyte infiltration in lung interstitium was less. Compared with IR group, MDA, MPO levels and W/D in IPC group decreased, but SOD increased （ all P 〈 0.05） ; compared with SO group, MDA, MPO levels and W/D in IPC and IR groups were all increased, SOD decreased （all P 〈 0.01 ）. Conclusion The ischemic postconditioning has the effect of alleviating lung ischemiareperfusion injury in rats and its mechanism is related to excessive production of oxygen free radicals after suppression of reperfusion.