Routledge P A, Shand D G, Barchowsky A, Wagner G, Stargel W W
Clin Pharmacol Ther. 1981 Aug;30(2):154-7. doi: 10.1038/clpt.1981.141.
The effects of myocardial infarction (MI) on lidocaine disposition were investigated in eight patients during a constant infusion of 2 mg/min. Plasma lidocaine binding and total plasma and free lidocaine concentrations were measured 12, 24, 36, and 48 hr after beginning therapy and were related to alpha 1-acid glycoprotein (AAG) concentrations. By 48 hr total plasma lidocaine and AAG concentrations had risen, as had plasma lidocaine binding. Because of enhanced binding, free lidocaine concentrations did not change significantly over this time. There was a correlation between AAG and the binding ratio for lidocaine (r = 0.87) and between AAG and total plasma lidocaine concentrations (r = 0.81). The data suggest that the rise in AAG seen after MI is responsible for enhanced plasma lidocaine binding and may, at least in part, be related to lidocaine cumulation.
在8名患者持续输注2毫克/分钟利多卡因的过程中，研究了心肌梗死（MI）对利多卡因处置的影响。在开始治疗后的12、24、36和48小时测量血浆利多卡因结合以及总血浆和游离利多卡因浓度，并将其与α1-酸性糖蛋白（AAG）浓度相关联。到48小时时，总血浆利多卡因和AAG浓度升高，血浆利多卡因结合也升高。由于结合增强，游离利多卡因浓度在此期间没有显著变化。AAG与利多卡因结合率之间存在相关性（r = 0.87），AAG与总血浆利多卡因浓度之间也存在相关性（r = 0.81）。数据表明，MI后出现的AAG升高是血浆利多卡因结合增强的原因，并且可能至少部分与利多卡因蓄积有关。
