论文部分内容阅读
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。可推断细胞凋亡是再灌注心肌损伤的重要机制
Objective: To investigate the relationship between myocardial ischemia-reperfusion injury and cardiomyocyte apoptosis. Methods: The model of myocardial ischemia-reperfusion injury (IRI) in rabbits with different ischemic time was prepared. The apoptosis of myocardial cells was detected. The activities of superoxide dismutase (SOD) and malondialdehyde (MDA) And serum myocardial enzyme levels. Results: The rate of apoptosis of cardiomyocytes was the highest at the time of reperfusion after ischemia 30min and 60min, accompanied by the marked decrease of plasma SOD activity and the increase of MDA content. Serum creatine phosphokinase (CK) content increased gradually with the prolongation of ischemia. CONCLUSION: Myocardial injury induced by reperfusion is influenced by myocardial ischemia time. Reperfusion after 30 ~ 60min ischemia is obviously accompanied by increased apoptosis of myocardial cells. Cardiomyocytes also have higher reperfusion after reperfusion Apoptosis rate, but more important is to aggravate cardiomyocyte necrosis. It can be inferred that apoptosis is an important mechanism of reperfusion myocardial injury