摘要
[目的]探讨利多卡因对兔肺缺血再灌注损伤的保护作用及可能机制.[方法]建立兔肺缺血再灌注动物模型.健康家兔30只,随机分为3组：A组为假手术组、B组为缺血再灌注组、C组为利多卡因处理＋缺血再灌注组,每组10只,每组分别于再灌注60 min时测定血浆丙二醛（MDA）、超氧化物歧化酶（SOD）、血红素氧合酶-1.[结果]再灌注60 min后,B和C组的肺组织W/D及IQA都较A组显著升高（P均〈0.01）,而C组的肺组织W/D及IQA都明显低于B组（P均〈0.01） B和C组的肺组织HO-1活性明显高于A组（P均〈0.01）,而与B组相比,C组的肺组织HO-1活性明显升高（P均〈0.01）.肺组织湿干重比（W /D）,光镜观察肺组织形态结构变化并测定肺损伤定量评价指标（IQA）.与A组相比,B组W/D、血浆MDA含量以及IQA显著升高（P均〈0.01）,而SOD含量显著降低（P〈0.01）.与B组相比,C组W/D、血浆MDA含量以及IQA明显降低（P均〈0.01）,而SOD含量明显升高（P〈0.01）.[结论]利多卡因可能通过抑制氧自由基损伤和通过增强肺组织HO-1活性而对肺缺血再灌注损伤产生保护作用.
[Objective]To explore the protective effects and mechanisms of lidocaine on lung ischemiareperfusion injury in rabbits. [Methods]The rabbit model of lung ischemia reperfusion was established. Thirty healthy rabbits were randomly divided into sham operation group（group A）, ischemic-reperfusion group（group B） and lidocaine plus ischemia-reperfusion group（group C） with 10 in each. Plasma malonaldehyde（MDA）, superoxide dismutase（SOD） and heme oxygenase-1 （HO-1） at 60rain after reperfusion in each group were measured. The ratio of warm and dry（W/D） in lung tissue and lung injury quantitative index（IQA） were measured. The light microscope was used to observe the change of lung tissue. [Results]After 60min reperfusion, the values of W/D and IQA in lung tissues of group B and group C were significantly higher than those of group A （all P〈0.01）, while the values of W/D and IQA in lung tissues of group C were significantly lower than those ofgroupB（allP〈0.01）. The activity of HO-1 in lung tissues of group BandgroupC was significantly higher than that of group A（all P〈0.01）. Compared with group B, HO 1 activity in group C increased significantly（all P 〈0.01）. Compared with group A, the W/D, MDA and IQA in group B obviously increased .（all P 〈0.01）, while SOD decreased significantly（ P 〈0.01 ）. Compared with group B, the W/D, plasma MDA and IQA in group C decreased significantly（all P 〈 0. 01 ）, while SOD increased significantly（ P〈0.01）. [Conclusion] Lidocaine has the protective effect on lung ischemia-reperfusion injury through inhibiting the injury of oxygen free radicals and increasing the activity of HO-1.
出处
《医学临床研究》
CAS
2011年第2期276-279,共4页
Journal of Clinical Research
