缺血预处理对猪肺缺血再灌注性损伤的保护机制

目的：探讨缺血预处理（IP）对猪肺缺血再灌注性损伤的保护机制。方法：将12只猪随机均分为对照组（C组）和实验组（IP组），测定肺静脉血中超氧化物歧化酶（SOD）和丙二醛（MDA）的量以反映IP对肺脂质过氧化的影响，并在光镜下检测肺泡内白细胞数目；用免疫组织化学法和RT-PCR法检测ICAM-1的表达，以探讨缺血预处理对肺缺血再灌注性损伤的保护机制。结果：IP组灌注后MDA明显低于C组，SOD明显高于C组（均P＜0.01）。镜下观察发现IP组肺损伤程度较轻。与C组相比，IP组ICAM-1无论在蛋白质水平还是mRNA水平上表达均明显下调（P＜0.01）。结论：IP对缺血再灌注性肺损伤具有保护作用。IP对肺损伤的保护作用机制可能与IP激活内源性抗氧化作用，灭活或减少氧自由基和下调ICAM-1表达有关。

Protective mechanism of ischemic preconditioning to the lung ischemia-reperfusion injury

Objective To determine the protective mechanism of preconditioning to the lung injury induced by ischemia-reperfusion. Methods Twelve pigs were randomly divided into 2 groups: control group (Group C) and ischemic preconditioning group (Group IP).The concentration of superoxide distrautase (SOD) and malondialdehyde (MDA) in circuit were checked before and after the perfusion to reflect the lipid peroxidation in the lungs. Left lung biopsies were performed immediately after the perfusion and 1 hour postperfusion for histologic examination. The ICAM-1 expression was assessed by immunohistochemical analysis with Envision method and the mRNA expression of ICAM-1 was analyzed by RT-PCR. Results SOD in Group IP was much higher than that in Group C (P<0.01). MDA in Group IP was much lower than that in Group C (P<0.01). The lung histologic examination showed that Group C was significantly more serious than Group IP in pulmonary edema,inflammatory cell infiltration,mild focal hemorrhage, and alveolar disruption. The expression of ICAM-1 of lung tissue obviously decreased in Group IP than that in Group C (P<0.01). The expression of ICAM-1 mRNA of lung tissue was significantly lower in Group IP than that in Group C (P<0.01). Conclusion Lung ischemic preconditioning can reduce the lung injury. The mechanisms of the protective effects of the IP may be related to the increase of SOD and the decrease of MDA. The preconditioning down-regulated the ICAM-1 expression is one of the mechanisms in reducing the lung injury.