缺血后处理拮抗鼠肺缺血再灌注损伤的机制研究

目的： 研究后处理对离体大鼠肺缺血再灌注损伤的影响并分析其可能的作用机制。方法: 建立离体大鼠肺缺血再灌注损伤模型。18只SD大鼠随机分为3组，每组6只。对照组（Con）缺血2 h后以Krebs-Henseleit buffer(KHB)液再灌注1 h；预处理（IPreC）组于缺血2 h前给予重复1次的5 min灌注和5 min缺血的处理，余同Con组；后处理（IPostC）组于缺血2 h后给予重复1次的5 min灌注和5 min缺血的后处理，即以KHB液行再灌注1 h。持续监测及记录肺动脉压（PAP），缺血前及再灌注末分别留取3 mL灌流液，缺血前、再灌注始及再灌注末分别切取约20 mg肺组织制作10%的组织匀浆，灌流液及肺组织匀浆用于测定白细胞介素-8（IL-8）、IL-10、丙二醛（MDA）及谷胱甘肽（GSH）的含量，再灌注结束测定肺湿／干重比（W/D）。结果: IPostC组和IPreC组的IL-8、MDA及W/D较Con组明显降低（P<0.05），IPostC组和IPreC组的IL-10较Con组明显升高（P<0.05）。结论: 缺血后处理能明显拮抗离体大鼠肺缺血再灌注损伤。

Protective effects of ischemic post-conditioning on ischemic reperfusion injury of lung in rats

AIM: To investigate the protective effects of ischemic post-conditioning on lung ischemic reperfusion injury in rats.METHODS: The model of ischemia-reperfusion injury in isolated buffer-perfused rat lungs was prepared. 18 rats were randomly allocated to three groups (n=6, each group). ① Control group: interrupted perfusion and ventilation for 2 h and followed by reperfusion for 1 h. ② Ischemic pre-conditioning (IPreC) group: ischemic post-conditioning (5R/5I, two times) at the onset of ischemia. ③ Ischemic post-conditioning (IPostC) group: ischemic post-conditioning (5R/5I, two times) between the end of ischemia and the beginning of reperfusion. Pulmonary arterial pressure (PAP) was measured continuously. 3 mL perfusate was obtained before ischemia and at the end of reperfusion respectively. Small pieces of lung tissue (about 20 mg) that cut before ischemia, at the beginning and end of reperfusion were made into homogenate. The concentration of interleukin-8 (IL-8), interleukin-10 (IL-10), malondialdehyde (MDA) and glutathione (GSH) were determined in the perfusate and homogenate. The wet to dry weight ratio (W/D) were also measured at the end of reperfusion.RESULTS: After 2 h ischemia and 1 h reperfusion, the levels of IL-8, MDA and W/D became significantly lower in IPostC and IPreC group than those in control group, accompanied by the increase in IL-10 activity (P<0.05).CONCLUSION: Ischemic post-conditioning reduces significantly ischemic reperfusion injury in isolated rat lungs.