摘要
目的探讨缺氧预适应对心肌细胞摄取与清除99Tcm甲氧基异丁基异腈(MIBI)和201Tl的影响。方法在原代培养心肌细胞基础上,建立缺氧预适应模型,通过台盼蓝染色方法计算细胞存活率。测定心肌细胞对99TcmMIBI和201Tl在不同时间点的参入和释放量,观察正常心肌细胞、经预适应后具有保护功能的心肌细胞以及缺氧/复氧后细胞对放射性药物的摄取情况。结果与缺氧/复氧组比较,缺氧预适应提高心肌细胞存活率20%[(7531±345)%和(5550±313)%,P<001]。正常心肌细胞浓聚99TcmMIBI达坪值的半峰值时间为128min,浓聚201Tl达坪值的半峰值时间为65min。与正常对照组比较,缺氧预适应增加心肌细胞摄取99TcmMIBI的量[(6103±170和4852±491)计数·min-1·mg-1protein,P<005],减少201Tl摄取量[(2120±202和3190±183)计数·min-1·mg-1protein,P<005]。预适应心肌细胞对99TcmMIBI和201Tl的清除均延迟。结论缺氧预适应对心肌细胞具有保护作用,预缺氧能影响心肌细胞对99TcmM?
Objective To study the effect of hypoxic preconditioning (HPC) on 99 TcmMIBI and 201 Tl kinetics in cultured neonatal rat cardiomyocytes Methods The protection of HPC was assayed on the model of hypoxia/reoxygenation(H/R) of cultured neonatal rat cardiomyocytes and the Trypan blue exclusion method was used to assess cell viability Normal, hypoxic preconditioning and hypoxia/reoxygenation cardiomyocytes groups were studied By measuring the diffused and released radioactivity of myocytes in different time intervals, the effect of HPC on 99 TcmMIBI and 201 Tl uptake and clearance kinetics in the myocytes was observed in various conditions Results Compared with H/R, the number of viable cells after HPC P <001] was greatly increased Normal cardiomyocytes showed uptake of 99*2/3TcmMIBI and 201 Tl to a plateau level with a halftime of 128 min and 65 min, respectively HPC caused a significant increase in uptake of 99 TcmMIBI mg-1protein to HPC group, (6 103170) countsmin-1mg-1protein; XP <005], but depressed 201 Tl uptake mg-1protein to HPC group, (2 120202) countsmin-1mg-1protein; P <005] The clearances of 99 TcmMIBI and 201 Tl were both retarded Conclusions These results suggested that the neonatal rat cardiomyocytes after HPC offered more capacity to tolerate the H/R damage and HPC could influence the 99 TcmMIBI and 201 Tl uptake and clearance
出处
《中华核医学杂志》
CSCD
北大核心
1999年第3期152-154,共3页
Chinese Journal of Nuclear Medicine
基金
陕西省自然科学基金