摘要
目的探讨缺血后处理对猪急性心肌梗死后的抗氧化作用.方法滇南小耳猪15只,随机数字表法分为3组,假手术组(S组,n=5),缺血再灌注组(IR组,n=5),缺血后处理组(IPC组,n=5).用球囊封堵冠脉建立猪闭胸式心肌梗死模型,术中监测心电及血压,测定缺血前、再灌注2 h及24 h血清超氧化物岐化酶(SOD)活力及丙二醛(MDA)含量,再灌注72 h采用2,3,5氯化三苯基氯四氮唑(TTC)染色确定心肌梗死面积.结果 (1)与假手术组相比,缺血再灌注组再灌注2 h,24 h MDA含量明显增加,SOD活力明显降低(P<0.05);与缺血再灌注组相比,缺血后处理组再灌注2 h,24 h MDA含量明显下降,SOD活力明显增加(P<0.05);(2)假手术组未发生心肌梗死,缺血再灌注组及缺血后处理组心肌梗塞的面积分别是(23.26±3.13)%,(10.89±2.02)%,缺血后处理组心肌梗塞面积较缺血再灌注组明显降低(P<0.05).结论缺血后处理对猪的心肌保护作用可能与其减少脂质过氧化产物MDA的含量,提高抗氧化物质SOD活性的抗氧化作用有关.
Objective To explore the anti-oxidative effects of ischemic postconditioning on the swine model of acute myocardial infarction.Methods Fifteen Diannan small-ear pigs were randomly divided into three groups:(1)Sham-operated(S,n=5)group;(2)Ischemia-reperfusion(I/R,n=5) group;(3)Ischemic postconditioning(IPC,n=5).The close-chest swine model of acute myocardial infarction was established by coronary occlusion with balloon angioplasty.ECG and blood pressure were monitored during the process.Serum biomarkers malondialdhyde(MDA)and superoxide dismutase(SOD)were assessed before ischemia,2 h after reperfusion and 24 h after reperfusion.After 72h of reperfusion,infarction size was measured by 2,3,5-triphenyltetrazolium chloride(TTC) staining.Results(1)Levels of serum MDA were all significantly reduced in IPC group compared with IR group(P<0.05),and the activities of SOD were enhanced(P<0.05);(2)In the IPC group,infarction size was smaller than that in IR group(P<0.05).Conclusions Ischemic postconditioning can protect myocardium against ischemia-reperfusion injury in swine,the mechanism may be related to decreasing oxygen free radical MDA and increasing the antioxidant activity of SOD.
出处
《昆明医科大学学报》
CAS
2012年第4期13-15,21,共4页
Journal of Kunming Medical University
基金
云南省应用基础研究面上项目基金资助项目(2007C243M)
关键词
缺血后处理
心肌
猪
缺血再灌注损伤
氧自由基
Ischemic Postconditioning
Myocardium
Swine
Ischemia-reperfusion injury
Oxygen free radical