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９９ＴｃｍＭＩＢＩ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％［（７５３１±３４５）％和（５５５０±３１３）％，Ｐ＜００１］。正常心肌细胞浓聚９９ＴｃｍＭＩＢＩ达坪值的半峰值时间为１２８ｍｉｎ，浓聚２０１Ｔｌ达坪值的半峰值时间为６５ｍｉｎ。与正常对照组比较，缺氧预适应增加心肌细胞摄取９９ＴｃｍＭＩＢＩ的量［（６１０３±１７０和４８５２±４９１）计数·ｍｉｎ－１·ｍｇ－１ｐｒｏｔｅｉｎ，Ｐ＜００５］，减少２０１Ｔｌ摄取量［（２１２０±２０２和３１９０±１８３）计数·ｍｉｎ－１·ｍｇ－１ｐｒｏｔｅｉｎ，Ｐ＜００５］。预适应心肌细胞对９９ＴｃｍＭＩＢＩ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９９ＴｃｍＭ? Objective To investigate the effects of hypoxic preconditioning on cardiomyocyte uptake and clearance of 99Tcm-methoxyisobutylisonitrile (MIBI) and 201Tl. Methods Based on primary cultured cardiomyocytes, hypoxia preconditioning model was established and cell viability was calculated by trypan blue staining. Determination of myocardial cells 99TcmMIBI and 201Tl at different time points of the participation and release, observed normal cardiomyocytes, after preconditioning with protective cardiomyocytes and hypoxia / reoxygenation cells after radiopharmaceuticals uptake. Results Compared with hypoxia / reoxygenation group, hypoxic preconditioning increased the survival rate of cardiomyocytes by 20% [(7531 ± 345)% and (5550 ± 3.13)%, P <001] . The concentration of 99TcmMIBI normal cardiomyocyte plateau peak value of the half-peak time of 12.8min, the concentration of 201Tl plateau value of the half-peak time of 65min. Compared with the normal control group, hypoxic preconditioning increased the uptake of 99TcmMIBI in myocardial cells [(6103 ± 170 and 4852 ± 491) counts · min-1 · mg-1protein, P <005] and decreased the intake of 201Tl [(2120 ± 202 and 3190 ± 183) counts · min-1 · mg-1 protein, P <005]. Preconditioning cardiomyocytes 99TcmMIBI and 201Tl clearance were delayed. Conclusions Hypoxic preconditioning has a protective effect on cardiomyocytes. Preconditioning hypoxia can affect the myocardial cells to 99Tcm M