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本文引用的文献

1
Protein binding of some non-steroidal anti-inflammatory drugs in rheumatoid arthritis.类风湿关节炎中某些非甾体抗炎药的蛋白质结合情况。
Clin Pharmacokinet. 1982 Jan-Feb;7(1):85-92. doi: 10.2165/00003088-198207010-00005.
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Quinine disposition kinetics.奎宁处置动力学。
Br J Clin Pharmacol. 1983 Oct;16(4):399-403. doi: 10.1111/j.1365-2125.1983.tb02184.x.
3
A human cytochrome P-450 characterized by inhibition studies as the sparteine-debrisoquine monooxygenase.一种通过抑制研究鉴定为司巴丁-异喹胍单加氧酶的人细胞色素P-450。
Can J Physiol Pharmacol. 1984 Jul;62(7):860-2. doi: 10.1139/y84-144.
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Clinical pharmacokinetics of antimalarial drugs.抗疟药物的临床药代动力学。
Clin Pharmacokinet. 1985 May-Jun;10(3):187-215. doi: 10.2165/00003088-198510030-00001.
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Pharmacokinetics and metabolism of quinidine in extensive and poor metabolisers of sparteine.
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Oxidation of quinidine by human liver cytochrome P-450.奎尼丁被人肝脏细胞色素P-450氧化。
Mol Pharmacol. 1986 Sep;30(3):287-95.
7
Quinidine and the identification of drugs whose elimination is impaired in subjects classified as poor metabolizers of debrisoquine.奎尼丁以及对那些被归类为异喹胍代谢缓慢者体内消除受损药物的鉴定。
Br J Clin Pharmacol. 1986 Dec;22(6):739-43. doi: 10.1111/j.1365-2125.1986.tb02969.x.
8
Characterization of rat and human liver microsomal cytochrome P-450 forms involved in nifedipine oxidation, a prototype for genetic polymorphism in oxidative drug metabolism.参与硝苯地平氧化的大鼠和人肝微粒体细胞色素P-450形式的表征,氧化药物代谢中遗传多态性的一个原型。
J Biol Chem. 1986 Apr 15;261(11):5051-60.
9
Characterization of the common genetic defect in humans deficient in debrisoquine metabolism.异喹胍代谢缺陷人类常见遗传缺陷的特征分析。
Nature. 1988 Feb 4;331(6155):442-6. doi: 10.1038/331442a0.
10
Clinical significance of the sparteine/debrisoquine oxidation polymorphism.司巴丁/异喹胍氧化多态性的临床意义
Eur J Clin Pharmacol. 1989;36(6):537-47. doi: 10.1007/BF00637732.

异喹胍氧化表型与奎宁药代动力学之间缺乏相关性。

Lack of relationship between debrisoquine oxidation phenotype and the pharmacokinetics of quinine.

作者信息

Wanwimolruk S, Chalcroft S

机构信息

School of Pharmacy, University of Otago, Dunedin, New Zealand.

出版信息

Br J Clin Pharmacol. 1991 Nov;32(5):617-20. doi: 10.1111/j.1365-2125.1991.tb03961.x.

DOI:10.1111/j.1365-2125.1991.tb03961.x
PMID:1954076
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1368640/
Abstract

The relationship between debrisoquine oxidation phenotype and the pharmacokinetics of quinine after a single dose (600 mg) of quinine sulphate was studied in eight extensive metabolizers (EM) and five poor metabolizers (PM). The mean elimination half-life of quinine in the PMs (10.2 +/- 1.6 (s.d.)h) was similar to that in the EMs (10.9 +/- 1.7 h). The oral clearance of quinine in the PM subjects was 0.092 +/- 0.021 l h-1 kg-1 and was not significantly different (P greater than 0.05) from that observed in the EM subjects (0.073 +/- 0.019 l h-1 kg-1). This suggests that even though quinine is extensively metabolized by oxidative biotransformation, this is carried out largely by P450 isoenzymes different from P450IID6 which oxidizes debrisoquine.

摘要

在8名快代谢者(EM)和5名慢代谢者(PM)中研究了异喹胍氧化表型与单次服用600毫克硫酸奎宁后奎宁药代动力学之间的关系。慢代谢者中奎宁的平均消除半衰期(10.2±1.6(标准差)小时)与快代谢者中的(10.9±1.7小时)相似。慢代谢受试者中奎宁的口服清除率为0.092±0.021升·小时⁻¹·千克⁻¹,与快代谢受试者中观察到的清除率(0.073±0.019升·小时⁻¹·千克⁻¹)相比无显著差异(P>0.05)。这表明,尽管奎宁通过氧化生物转化被广泛代谢,但这主要是由不同于氧化异喹胍的P450IID6的P450同工酶进行的。