Suhara T, Farde L, Halldin C, Någren K, Karlsson P
Karolinska Institute, Department of Neuroscience, Karolinska Hospital, Stockholm, Sweden.
Ann Nucl Med. 1996 Feb;10(1):85-8. doi: 10.1007/BF03165058.
The toxic properties of cocaine are related to both the central and peripheral effects. To identify possible lethal mechanisms and the accumulation of cocaine in various organs, the effects of cocaine on [11C]norepinephrine and cocaine congener [11C] beta-CIT uptake in Cynomolgus monkeys were measured by positron emission tomography (PET). Cocaine (5 mg/kg) noticeably inhibited [11C]norepinephrine uptake in the heart. The uptake of [11C] beta-CIT in the heart and lung was reduced by pretreatment with cocaine. There was a significant uptake in the liver which was increased following cocaine pretreatment. The results of this study confirm that cocaine blocks the neuronal uptake of norepinephrine in sympathetic nerve terminals in the myocardium. The effect of cocaine on [11C] beta-CIT uptake indicates that the binding sites in the heart and lung are saturable, while the uptake mechanism in the liver is different from those of the heart and lung.
可卡因的毒性特性与中枢和外周效应均有关。为了确定可能的致死机制以及可卡因在各个器官中的蓄积情况，通过正电子发射断层扫描（PET）测量了可卡因对食蟹猴体内[11C]去甲肾上腺素和可卡因同系物[11C]β-CIT摄取的影响。可卡因（5毫克/千克）显著抑制了心脏中[11C]去甲肾上腺素的摄取。预先使用可卡因可降低心脏和肺中[11C]β-CIT的摄取。肝脏中有显著摄取，且在可卡因预处理后增加。本研究结果证实，可卡因可阻断心肌交感神经末梢中去甲肾上腺素的神经元摄取。可卡因对[11C]β-CIT摄取的影响表明，心脏和肺中的结合位点是可饱和的，而肝脏中的摄取机制与心脏和肺不同。
