Katagiri E, Sakai M, Horikawa H
Department of Anesthesia, Yamagata University School of Medicine.
Masui. 1991 Jan;40(1):80-90.
Lidocaine pharmacokinetics were studied using perfused rat livers under several conditions. 1) In the low perfusion group (perfusion rate = 1/2 of control group), the elimination rate constant and clearance of lidocaine in the first phase were reduced, but in the second phase, metabolism of lidocaine was more active than in other groups. 2) High albumin concentration in the perfusate did not significantly affect lidocaine metabolism. 3) Low pH of the perfusate (pH = 7.10) did not affect the metabolism of lidocaine. 4) Acute and chronic liver damage inhibited the lidocaine metabolism, which may be due to decreases in viable hepatocytes, effective hepatic blood flow and mitochondrial P-450. 5) Halothane in the concentration of 2.5% reduced the lidocaine metabolism. This was probably due to inhibition of hepatocyte activity by halothane because increases in GOT, LDH and lactate in the perfusate and a decrease in the O2 consumption by the rat liver were observed.
在多种条件下，使用灌注大鼠肝脏研究利多卡因的药代动力学。1）在低灌注组（灌注速率=对照组的1/2）中，利多卡因在第一阶段的消除速率常数和清除率降低，但在第二阶段，利多卡因的代谢比其他组更活跃。2）灌注液中高白蛋白浓度对利多卡因代谢无显著影响。3）灌注液低pH值（pH = 7.10）不影响利多卡因代谢。4）急性和慢性肝损伤抑制利多卡因代谢，这可能是由于存活肝细胞、有效肝血流量和线粒体P-450减少所致。5）2.5%浓度的氟烷降低了利多卡因代谢。这可能是由于氟烷抑制肝细胞活性，因为观察到灌注液中谷草转氨酶、乳酸脱氢酶和乳酸增加，以及大鼠肝脏耗氧量减少。
