N-Acetylprocainamide: An Active Metabolite of Procainamide 1
N-Acetylprocainamide: An Active Metabolite of Procainamide 1
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N-乙酰基普鲁卡因酰胺：普鲁卡因酰胺 1 的活性代谢物
DOI：
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发表时间：
1974
期刊：
影响因子：
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通讯作者：
R. Sevy
中科院分区：
文献类型：
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作者：
D. Drayer;M. Reidenberg;R. Sevy
摘要在接受普鲁卡因胺治疗的四名患者的血浆样本中均检测到N-乙酰普鲁卡因胺。从薄层色谱数据中鉴定了该代谢物，并通过气相色谱-质谱联用分析对其进行了鉴定。给药后，SD大鼠全血中也检测到该代谢物。当给42至49天的ICR雄性小鼠注射NaPA·HCI时，可防止由深度氯仿麻醉和由此导致的低氧引起的粗大室颤。NaPA·HCl可降低乌头碱诱发的3只犬心房扑动或房性心动过速伴不同程度房室传导阻滞的心律失常。TLC分析表明，在药理试验期间，小鼠、狗和大鼠没有去乙酰化纳帕酮。研究发现，与PA相比，NAPA在Spraogue-Dawley大鼠体内产生的铁血红蛋白更少。
Summary N-Acetylprocainamide has been detected in the plasma samples of each of four patients receiving procainamide. The metabolite was identified from tlc data and its identity confirmed by gas chomatographic-mass spectroscopic analysis. The metabolite was also detected in the whole blood of Sprague-Dawley rats after administration of PA. NAPA · HCI when injected ip into 42- to 49- day-old ICR male mice prevented coarse ventricular fibrillation caused by deep chloroform anesthesia and resultant hypoxia. NAPA · HCl reduced aconitine-induced arrhythmia to atrial flutter or atrial tachycardia with varying degrees of A-V block in three dogs. Analysis by tlc indicated that the mice, dogs, and rats did not deacetylate NAPA during the period of pharmacologic testing. NAPA was found to cause less ferrihemoglobin in Sprague-Dawley rats than did PA.