临床评估carbon-11-phenylephrine: MAO-sensitive心脏交感神经元的标志。

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引用

Raffel DM、小Corbett del Rosario RB, Gildersleeve DL,焦立中PC, Schwaiger M,维兰德DM

临床评估carbon-11-phenylephrine: MAO-sensitive心脏交感神经元的标志。

J诊断。1996年12月,37(12):1923 - 31所示。

PubMed ID
8970507 (在PubMed
]
文摘

拟交感神经药物苯肾上腺素最近一直用11 c标记用于宠物研究心脏交感神经支配的。先前的报道使用隔离灌注大鼠心脏模型表明,苯肾上腺素代谢的intraneuronal单胺氧化酶(MAO)。这份报告比较了成像特点,神经选择性和动力学(-)- c[11]苯肾上腺素(苯酚的)结构相似但MAO-resistant模拟(-)- c [11] -meta-hydroxyephedrine (HED),建立心脏神经标记。方法:14个健康的志愿者进行了研究与宠物和苯酚的。十与HED配对研究;四的10第二次扫描每个示踪去郁敏口服后,选择性神经传输拦截器。血流动力学和心电图描记的反应都是被监控的。完整的放射性示踪剂和放射性标记的代谢物浓度测定在宠物研究从静脉血样。心肌保留指数计算的示踪剂。结果:没有血流动力学或心电图描记的效果观察与示踪剂。 PHEN showed reduced myocardial retention at 50 min compared to HED; however, image quality and uniformity of distribution were comparable. PHEN cleared from myocardium with a mean half-time of 59 +/- 5 min, while myocardial levels of HED remained constant. PHEN metabolites appeared in the blood approximately three times faster than HED metabolites. Desipramine pretreatment markedly reduced (> 60%) myocardial retention of both PHEN and HED. CONCLUSION: PHEN provides PET images of human heart comparable in quality and uniformity to HED. Like HED, PHEN localizes in the sympathetic nerves of the heart. However, the more rapid efflux of PHEN, that is likely mediated by MAO, may provide information on the functional status of cardiac sympathetic neurons unobtainable with HED.

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药物酶
药物 生物 药理作用 行动
苯肾上腺素 胺氧化酶(flavin-containing) 蛋白质 人类
未知的
底物
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