Yoneda I
Department of Anethesiology, National Defense Medical College, Tokorozawa.
Masui. 1993 May;42(5):652-63.
The purpose of the first study was to identify the relationship between reflex sympathetic nerve activity and plasma concentration of lidocaine. Lidocaine was infused in 4 different doses: 2 mg.kg-1 bolus + 100 micrograms.kg-1 x min-1, 3 mg.kg-1 bolus + 200 micrograms.kg-1 x min-1, 6 mg.kg-1 bolus + 400 micrograms.kg-1 x min-1 and 12 mg.kg-1 bolus + 800 micrograms.kg-1 x min-1. Baroreflex depressor and pressor tests using sodium nitroprusside (5-10 micrograms.kg-1) and phenylephrine (2-4 micrograms.kg-1) were performed before and at 10 min after the start of lidocaine infusion. Plasma lidocaine concentrations determined by HPLC revealed that its steady-state levels were maintained during the baroreflex tests. Baroreflex sensitivity was preserved at clinical concentrations of lidocaine (< 5 micrograms.ml-1). However, baroreflex was significantly attenuated when plasma lidocaine concentrations were above seizure levels (> 10 micrograms.ml-1). This result indicates that hemodynamic derangement observed in the lidocaine-induced CNS toxicity is, at least in part, due to the attenuated arterial baroreflex. In the second study, the author evaluated the effect of respiratory acidosis and alkalosis on the baroreflex with or without lidocaine infusion (2 mg.kg-1 + 100 micrograms.kg-1 x min-1). Respiratory acidosis (PaCO2: 65.6 +/- 3.4) enhanced the baroreflex significantly, but lidocaine infusion abolished this acidosis-induced enhancement. The author concludes that hypercarbia should be avoided in patients receiving intravenous lidocaine infusion.
第一项研究的目的是确定反射性交感神经活动与利多卡因血浆浓度之间的关系。以4种不同剂量输注利多卡因：2mg·kg⁻¹静脉推注+100μg·kg⁻¹×min⁻¹、3mg·kg⁻¹静脉推注+200μg·kg⁻¹×min⁻¹、6mg·kg⁻¹静脉推注+400μg·kg⁻¹×min⁻¹和12mg·kg⁻¹静脉推注+800μg·kg⁻¹×min⁻¹。在利多卡因输注开始前及开始后10分钟，使用硝普钠（5 - 10μg·kg⁻¹）和去氧肾上腺素（2 - 4μg·kg⁻¹）进行压力感受性反射降压和升压试验。通过高效液相色谱法测定的血浆利多卡因浓度显示，在压力感受性反射试验期间其稳态水平得以维持。在利多卡因临床浓度（<5μg/ml）时压力感受性反射敏感性得以保留。然而，当血浆利多卡因浓度高于惊厥水平（>10μg/ml）时，压力感受性反射显著减弱。该结果表明，利多卡因诱导的中枢神经系统毒性中观察到的血流动力学紊乱至少部分归因于动脉压力感受性反射减弱。在第二项研究中，作者评估了呼吸性酸中毒和碱中毒对有或无利多卡因输注（2mg·kg⁻¹+100μg·kg⁻¹×min⁻¹）时压力感受性反射的影响。呼吸性酸中毒（动脉血二氧化碳分压：65.6±3.4）显著增强了压力感受性反射，但利多卡因输注消除了这种酸中毒诱导的增强作用。作者得出结论，接受静脉输注利多卡因的患者应避免高碳酸血症。
