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为研究心肌细胞活性对~(99m)Tc-sestamibi浓聚的影响,作者复制了猪冠状动脉阻塞模型.分别于阻塞前30min(第一组)、阻塞开始后15min(第二组)及再灌注后30min(第三组)静脉注射~(99m)Tc-sesta-mibi(185MBq),然后分别进行平面显像并测定非缺血区、缺血区及梗塞区心肌的肌酸激酶(CK)含量、~(99m)Tc-sestamibi的放射性活度,用伊文氏兰及TTC染色对非缺血区、缺血区及梗塞区进行心肌血流分析.结果:三组间各期血液动力学数据(包括心率及平均动脉压)无显著性差异;三组缺血区的CK含量均明显低于非缺血区,梗塞区降低更显著.非缺血区、缺血区及梗塞区的~(99m)Tc放射性活度分别为:第一组1.00,0.92±0.11及0.62±0.14;第二组1.00,0.33±0.02及0.37±0.03;第三组1.00,
To investigate the effect of cardiomyocyte activity on the accumulation of ~ (99m) Tc-sestamibi, we cloned a model of porcine coronary artery occlusion (CAD) in the first 30 min (group 1), 15 min (group 2) Thymidine (99m) Tc-sesta-mibi (185MBq) was injected intravenously 30min later (the third group), and then plain imaging was performed and the creatine kinase (CK) content in the myocardium in non- ischemic, , ~ (99m) Tc-sestamibi radioimmunoassay, myocardial perfusion analysis was performed on non-ischemic, ischemic and infarcted regions using Evangelion and TTC staining.Results: The hemodynamic data of all groups Including heart rate and mean arterial pressure). There was no significant difference in the content of CK between ischemic and ischemic areas in all three groups ) Tc radioactivity were 1.00,0.92 ± 0.11 and 0.62 ± 0.14 for the first group, 1.00, 0.33 ± 0.02 and 0.37 ± 0.03 for the second group,