本研究利用大白鼠腦細胞探討鎝-99m-d，1-HMPAO滯留腦細胞的機制，實驗的方法為使用大白鼠活體實驗與試管內實驗等兩種方式進行，並比較同系列異構物鎝-99m-meso-HMPAO與鎝-99m-PnAO的腦細胞內分佈的異同。鎝-99m-d，1-HMPAO與鎝-99m-m的o-HMPAO進入腦細胞後可分佈於粒線體，且與組織的存活度有關:而鎝-99m-PnAO則只有極低 比例能分佈於粒線體。由化學實驗得鎝-99m-d，1-HMPAO於般性條件下較鎝-99m-meso-HMPAO容易酸水解，在pH11直極低的粒線體中，鎝-99m-d，1-HMPAO的比例高於鎝-99m-meso-HMPAO。鎝-99m-d，1-HMPAO分佈於腦細胞粒線體內可能為其滯留腦細胞的主要機制。

The intracellular distributions of 99mTc-d，I-HMPAO， 99mTc_ meso-HMPAO and 99mTc-PnAO in rat brains were explored in vivo and in vitro. 99mTc-d，I-HMPAO and 99mTc_ meso-HMPAO were found to distribute in the mitochondria of rat brain cells with radioactivity prominent throughout the whole brain (ca. 33.1 % and 26.5%， respectively) at 10 min post-injection in the in vivo study. Binding to the cerebral mitochondria appeared sensitive to tissue viability or other physiological parameters. This sensitivity was evidenced by the corresponding in vitro study which revealed significantly less radioactivity than that of in vivo in the mitochondria. The binding of both 99mTc-HMPAO diastereomers to the mitochondria was stable after washing with SEH buffer. Extremely low radioactivity of 99mTc-PnAO (-10%) was found in the mitochondria in both in vivo and in vitro studies; the complex proved to be loosely bound and was readily washed out with SEH buffer. The preferential internalization of 99mTc-d，I-HMPAO and 99mTc-mesoHMPAO in the mitochondria could be a step towards an enzymatic degradation in the viable brain cells， for instance through acid hydrolase. The difference in the extent of binding between two 99mTc-HMPAO diastereomers might depend on acid susceptibility， which might be related to the enzymatic acid hydrolysis in the mitochondria. From this study， intracellular binding to mito- chondria may be the major mechanism for trapping 99mTc-HMPAO in the brain cells.