Jacobi J, McGory R W, McCoy H, Matzke G R
Clin Pharm. 1983 Jan-Feb;2(1):54-7.
The hemodialysis clearance and protein binding of lidocaine was determined in two acutely ill patients with end-stage renal disease. Patient A was a 74-year-old white man admitted for severe thrombocytopenia; lidocaine was started to control ventricular tachycardia. Patient B was a 66-year-old white man admitted for a myocardial infarction (MI); prophylactic treatment with lidocaine was begun after a second MI. Lidocaine hemodialysis clearance was evaluated during a five-hour dialysis procedure. Paired arterial and venous blood samples for lidocaine concentrations were collected at the midpoint of each hour of dialysis. Before dialysis and two hours after dialysis, venous samples were collected and assayed for alpha-1-acid glycoprotein (AAG) and lidocaine. The hemodialysis clearance of total and unbound lidocaine was calculated. The total amount of lidocaine removed was 8.9 and 12.5 mg for patients A and B, respectively. These amounts represented the removal of 5.6 and 2.8% of the total lidocaine dose administered to patients A and B, respectively, during the dialysis procedure. For patient A, the mean plasma dialysis clearance (Clp) was 28.2 +/- 6.3 ml/min for total lidocaine and 41.3 +/- 15.6 ml/min for unbound lidocaine. The Clp could not be calculated for patient B. The mean dialysate clearance (Cld) of total lidocaine was 28.6 +/- 7.8 and 26.3 +/- 6.5 ml/min for patients A and B, respectively. The Cld of unbound lidocaine was 42.7 +/- 6.7 and 44.5 +/- 9.9 for patients A and B, respectively. Although both patients A and B had substantial elevations in AAG concentrations (254 and 247 mg/dl, respectively), they exhibited high lidocaine unbound fractions of 0.55 and 0.68 before dialysis. The lidocaine unbound fraction was further increased in patient A after fat emulsion infusion to 0.80 and in patient B after heparin administration to 0.90. The clearance of lidocaine by hemodialysis in these two patients was negligible and clinically unimportant. No dose adjustment or supplementation was required after hemodialysis.
在两名患有终末期肾病的急性病患者中测定了利多卡因的血液透析清除率和蛋白结合率。患者A是一名74岁的白人男性，因严重血小板减少症入院；开始使用利多卡因来控制室性心动过速。患者B是一名66岁的白人男性，因心肌梗死（MI）入院；在第二次心肌梗死后开始使用利多卡因进行预防性治疗。在为期5小时的透析过程中评估了利多卡因的血液透析清除率。在透析的每个小时的中点采集成对的动脉和静脉血样以测定利多卡因浓度。在透析前和透析后两小时，采集静脉血样并测定α-1-酸性糖蛋白（AAG）和利多卡因。计算了总利多卡因和未结合利多卡因的血液透析清除率。患者A和B的利多卡因清除总量分别为8.9毫克和12.5毫克。这些量分别占透析过程中给予患者A和B的总利多卡因剂量的5.6%和2.8%。对于患者A，总利多卡因的平均血浆透析清除率（Clp）为28.2±6.3毫升/分钟，未结合利多卡因的Clp为41.3±15.6毫升/分钟。患者B的Clp无法计算。患者A和B的总利多卡因平均透析液清除率（Cld）分别为28.6±7.8毫升/分钟和26.3±6.5毫升/分钟。患者A和B的未结合利多卡因的Cld分别为42.7±6.7和44.5±9.9。尽管患者A和B的AAG浓度均大幅升高（分别为254毫克/分升和247毫克/分升），但他们在透析前的利多卡因未结合分数分别为0.55和0.68。在患者A输注脂肪乳剂后，利多卡因未结合分数进一步升高至0.80，在患者B给予肝素后升至0.90。这两名患者通过血液透析对利多卡因的清除率可忽略不计，在临床上并不重要。透析后无需调整剂量或补充药物。
