Olsen H, Koppang E, Alvan G, Mørland J
Department of Clinical Pharmacology, University Hospital, Tromsø, Norway.
Ther Drug Monit. 1994 Aug;16(4):337-40. doi: 10.1097/00007691-199408000-00001.
The elimination of the muscle relaxant drug, carisoprodol, was examined in 10 healthy volunteers after an oral dose of 700 mg. In nine subjects, carisoprodol was rapidly eliminated, with a mean half-life of 99 +/- 46 min, and extensively converted to meprobamate. Within 2.5 h after carisoprodol intake, meprobamate serum concentrations exceeded those of carisoprodol. Serum levels of meprobamate recorded (15-25 mumol/L) indicate that meprobamate might contribute to the effect(s) of carisoprodol. One subject eliminated carisoprodol with an overall half-life of 376 min, and only small amounts of meprobamate were recorded. This subject was found to be a poor metabolizer of mephenytoin. In spiked human sera, protein binding of carisoprodol was in the range of 41-67%, whereas meprobamate was bound to a lesser extent, 14-24%.
在10名健康志愿者口服700毫克肌肉松弛药物卡立普多后，对其消除情况进行了研究。在9名受试者中，卡立普多迅速消除，平均半衰期为99±46分钟，并广泛转化为甲丙氨酯。在摄入卡立普多后2.5小时内，甲丙氨酯的血清浓度超过了卡立普多。记录的甲丙氨酯血清水平（15 - 25μmol/L）表明甲丙氨酯可能对卡立普多的效应有贡献。一名受试者消除卡立普多的总体半衰期为376分钟，仅记录到少量甲丙氨酯。发现该受试者是美芬妥因的代谢不良者。在加标的人血清中，卡立普多的蛋白结合率在41% - 67%范围内，而甲丙氨酯的结合程度较低，为14% - 24%。
