Saranteas Theodosios, Mourouzis Constantinos, Anagnostopoulou Sophia, Danis Kostas, Tachmintzis Annete, Rallis George
Department of Pharmacology, Medical School, University of Athens, Athens, Greece.
J Oral Maxillofac Surg. 2006 Jun;64(6):892-5. doi: 10.1016/j.joms.2005.11.042.
This study was designed to investigate the disposition of (14)C-lidocaine in serum and tissues in rats with liver dysfunction.
Eighteen male rats were randomly divided into 2 groups. Group A was considered as control while group B underwent liver damage by administrating CCl(4) 0.4 mg/kg twice a week for 6 weeks. Both groups received 5 doses of 2.5 mg/kg lidocaine mixture (labeled (14)C-lidocaine and nonlabeled). The rats were killed 2 hours after the last dose. Total lidocaine levels ((14)C-lidocaine and (14)C-lidocaine metabolite concentrations) as well as the percent of total lidocaine-bound fractions in tissues were measured.
(14)C-lidocaine concentrations were significantly increased in the serum (9.4+/-0.4 microg/mL), heart (7.8+/-2 microg/gL), and mandible (0.97+/-0.01 microg/g) in diseased rats as compared with normal rats (serum, 5.3+/-1.7 microg/mL; heart, 4.2+/-0.9 microg/g; mandible, 0.68+/-0.02 microg/g, respectively). (14)C-lidocaine bound fractions in the mandible and heart did not show any significant differences between the 2 groups. Instead, (14)C-lidocaine bound fractions in serum were significantly reduced in diseased animals as opposed to normal ones.
We concluded that liver dysfunction can modify (14)C-lidocaine concentrations in the serum and tissues without altering the lidocaine binding properties in the mandible and heart.
本研究旨在调查肝功能不全大鼠血清和组织中（14）C-利多卡因的分布情况。
18只雄性大鼠随机分为2组。A组作为对照组，B组每周两次给予0.4mg/kg四氯化碳，持续6周以造成肝损伤。两组均接受5剂2.5mg/kg利多卡因混合物（标记的（14）C-利多卡因和未标记的）。最后一剂后2小时处死大鼠。测量总利多卡因水平（（14）C-利多卡因和（14）C-利多卡因代谢物浓度）以及组织中总利多卡因结合部分的百分比。
与正常大鼠相比（血清分别为5.3±1.7μg/mL；心脏，4.2±0.9μg/g；下颌骨，0.68±0.02μg/g），患病大鼠血清（9.4±0.4μg/mL）、心脏（7.8±2μg/gL）和下颌骨（0.97±0.01μg/g）中的（14）C-利多卡因浓度显著升高。两组下颌骨和心脏中的（14）C-利多卡因结合部分没有显示出任何显著差异。相反，与正常动物相比，患病动物血清中的（14）C-利多卡因结合部分显著降低。
我们得出结论，肝功能不全可改变血清和组织中（14）C-利多卡因的浓度，而不改变下颌骨和心脏中利多卡因的结合特性。
