缺血后处理对肺再灌注损伤中脂质过氧化反应的调整

Adjustment of lipid peroxidation after lung reperfusion injury by ischemic postconditioning

目的:缺血后处理即在全面恢复再灌注前反复短暂多次预再灌、停灌,探讨缺血后处理对在体大鼠肺缺血再灌注损伤的脂质过氧化反应的影响。方法:实验于2004-05/06在汕头大学医学院附属肿瘤医院中心实验室完成。通过阻断左肺门建立大鼠在体左肺缺血再灌注模型,将24只健康雌性SD大鼠随机分为①假手术组8只:持续灌注105min。②缺血再灌注组8只:缺血45min,再灌注60min。③缺血后处理组8只:缺血45min后,短暂再灌注1min,缺血1min,反复5次,然后再全面恢复灌注60min。试验结束后处死动物,切取新鲜肺左叶组织制成100g/L组织匀浆,测定丙二醛含量用硫代巴比妥酸比色法,测定超氧化物歧化酶活性用黄嘌呤氧化酶法(羟胺法)。结果:3组24只动物均进入结果分析。①肺组织丙二醛含量测定结果:假手术组为(0.934±0.086)μmol/g,对照组为(1.230±0.169)μmol/g,缺血后处理组为(1.064±0.090)μmol/g,缺血后处理组与对照组相比明显降低(P<0.05)。②超氧化物歧化酶活性测定结果:假手术组为(2.838±0.509)μkat/g,对照组为(1.183±0.222)μkat/g,缺血后处理组为(2.008±0.298)μkat/g,缺血后处理组与对照组相比显著升高(P<0.01)。结论:对照组与假手术组相比,肺组织经历45min缺血60min再灌注后丙二醛含量明显升高,抗自由基酶类超氧化物歧化酶活性显著下降,说明再灌注期肺组织脂质过氧化反应增强,抗氧化能力降低。缺血后处理组较对照组肺组织中脂质代谢产物丙二醛含量下降,抗自由基酶超氧化物歧化酶活性增加,表明缺血后处理可减轻在体大鼠肺缺血再灌注损伤的脂质过氧化反应而产生肺保护作用。

AIM: Ischemic postconditioning is to give repeated and transient prereperfusion and cease of perfusion for several times before comprehensive recovery reperfusion. This paper aims to investigate the effect of ischemic postconditioning on lipid peroxidation in rats after in vivo lung reperfusion injury. METHODS: The experiment was completed in the central laboratory of the Tumor Hospital affiliated to the Medical College of Shantou University between May and June 2004. Rat models of in vivo left lung reperfusion injury were induced by occluding hilum of left lung, 24 healthy female SD rats were randomly divided into 3 groups: ①shamoperated group (n=8): continuous perfusion for 105 minutes; ② ischemic-reperfusion group (n=8): ischemia for 45 minutes and reperfusion for 60 minutes; ③ ischemic postconditioning group (n=8): ischemia for 45 minutes, transient reperfusion for 1 minute, ischemia for 1 minute, which were repeated for 5 times, and then recovered to comprehensive reperfusion for 60 minutes. The rats were killed after the experiment, the fresh left lung lobe tissues were taken and prepared to 100 g/L tissue homogenate to detect the content of malondialdehydewith thiobarbituric acid chromatometry, and the activity of superoxide dismutase with the method of xanthine oxidase (hydroxylamine method). RESULTS: All the 24 rats in the 3 groups were involved in the analysis of results. ① The content of malondialdehyde in lung tissue: It was (0.934±0.086) μmol/g in the sham-operated group, (1.230±0.169) μmol/g in the control group and (1.064±0.090) μmol/g in the ischemia postconditioning group; It was obviously decreased in the ischemia postconditioning group as compared with that in the control group (P < 0.05). ② The activity of superoxide dismutase: It was (2.838±0.509) μkat/g in the sham-operated group, (1.183±0.222)μkat/g in the control group and(2.008±0.298) μkat/g in the ischemia postconditioning group; It was obviously increased in the ischemia postconditioning group as compared with that in the control group (P < 0.01). CONCLUSION: Compared the control group with the sham-operated group, after ischemia for 45 minutes and reperfusion for 60 minutes in the lung tissue, the content of malondialdehyde is obviously increased, and the activity of anti-free radical enzyme superoxide dismutase is significantly decreased, it is indicated that the lipid peroxidation reaction in the lung tissue at reperusion is enhanced, and the anti-oxidative ability is reduced. Compared with the control group, the content of malondialdehyde, which is the lipid metabolite, in lung tissue is obviously decreased and the activity of anti-free radical enzyme superoxide dismutase is increased in the ischemia postconditioning group, it is indicated that ischemia postconditioning can relieve the lipid peroxidation reaction in rats with in vivo lung ischemia reperfusion injury, and then plays a role in protecting lung.