摘要
应用实验动物犬观察了氧自由基清除剂超氧化物岐化酶(Superoxide dismutase,SOD)和黄嘌呤氧化酶抑制剂别嘌呤醇(Allopurinol,ALLO)对冠脉阻断后再灌注心肌梗塞范围以及心肌琥珀酸脱氢酶活性和定位分布的影响。结果:冠脉阻断60 min再通120min组心肌梗塞量为11.05±4.28%,SOD防治组0.81±0.64%,ALLO防治组2.45±1.83%。冠脉阻断90 min再通120 min组心肌梗塞量为21.41±1.86%,SOD防治组为2.93±0.80%,ALLO防治组为3.54±1.23%。各防治组与相应对照组比较差别显著(P<0.01)。经SOD或ALLO防治后,再灌注区心肌琥珀酸脱氢酶活性和定位分布均得到保护,近于正常水平,防止了再灌注损伤的发生,表明冠脉再灌注损伤是由氧自由基所致,黄嘌呤氧化酶是氧自由基的主要来源。
The present experiments were performed to investigate the influence ofsuperoxide dismutase (SOD), an oxygen free radical scavenger and allopurinol(ALLO), a xanthine oxidase inhibitor on infarct size and alterations ofsuccinic dehydrogenase (SDH) activity and distribution induced by occlusionof left anterior descending coronary artery (LAD) followed by reopening. Theresults showed that in the group of occlusion of LAD for 60 min followed byreopening for 120 min, the infarct size expressed as a percentage of leftventricular and septal mass (g) was 11.05±4.28% (X±s), but 0.81±0.64%and 2.45±1.83% after treatment with SOD and ALLO respectively, in thegroup of occlusion of LAD for 90 min followed by reopening for 120 min, theinfarct size was 21.45±1.86%, but 2.53±0.80% and 3.54±1.23% aftertreatment with SOD and ALLO. The difference was significant betweencontrol and experimental gronp by statisical t test (P<0.01). SDH activityand distribution were well protected from hazardous effect of postischemicreperfusion with intervention of SOD or ALLO. In conclusion, the postischemicreperfusion injury to myocardium was caused by oxygen free radicals generatedmainly by myocardial xanthine oxidase.
出处
《中国医科大学学报》
CAS
CSCD
1991年第4期276-280,共5页
Journal of China Medical University
关键词
心肌缺血
再灌注损伤
自由基
reperfusion
oxygen free radical
succinic dehydrogenase
superoxide dismutase
allopurinol
