摘要
目的 :探讨心肌缺血 -再灌注损伤和心肌细胞凋亡的关系。方法 :制备不同缺血时间的家兔心肌缺血 -再灌注损伤 (IRI)的模型 ,检测心肌细胞凋亡情况 ,同时测定血浆过氧化物歧化酶(SOD)活性、丙二醛 (MDA)浓度和血清心肌酶水平。结果 :心肌细胞凋亡率以缺血30min及60min后再灌注时最高 ,同时伴有血浆SOD活性明显降低和MDA含量明显增高。血清肌酸磷酸激酶 (CK)含量随缺血时间延长呈逐渐增高趋势。结论 :再灌注加重心肌损伤受心肌缺血时间的影响 ,以30～60min缺血后的再灌注为明显 ,与心肌细胞凋亡加重同时并存 ;缺血时间长后再灌注也有较高的心肌细胞凋亡率 ,但更主要是加重心肌细胞坏死。
Objective: To study the relationship between myocardial-repefusion injury and apoptosis. Method: Models of myocardial-reperfusion injury were made in rabbits at various ischemic times. The presence of apoptotic myocytes was demonstrated by terminal deoxynucleotidyl transferase-mediated dUPT nich end labeling (TUNEL). The activities of plasma superoxide dismutase (SOD), the contents of serum malonic aldehyde (MDA) and the serum cardiac enzymes, including creatine kinase (CK) were checked at the same time. Results: The apoptotic rate of myocytes in ischemia was the highest at 30 min. and 60 min. after reperfusion. Plasma activities of SOD obviously decresed and the levels of serum MDA were also higher under those circumstances (P<0.01 or 0.05). The contents of serum CK were observed to rise gradually according to the periods of myocardial ischemia, i.e., the longer myocarial ischemia, the higher the CK contents. Conclusion: The study indicates that reperfusion after long ischemia (60 min. and over) might chiefly cause necrosis but not apoptosis in myocytes. The realy reperfusion injury mostly occurred in reperfusion 30-60 min. after ischemia accompanied with a high apoptotic rate. It can be inferred that apoptosis is an important pathogenesis of myocardial reperfusion injury due to the co-existing of both the myocardial injury and myocyte apoptosis caused intensely by reperfusion.
出处
《海南医学院学报》
CAS
2000年第3期129-133,共5页
Journal of Hainan Medical University
关键词
心肌缺血
再灌注损伤
细胞凋亡
自由基
Myocardial ischemia
myocardial reperfusion injury
apoptotic rate
free radical
