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논문 기본 정보

자료유형
학술저널
저자정보
Lee, In-Kyung (Department Pharmaceutics, College of Pharmacy, Seoul National University) Lee, Young-Mi (Department Pharmaceutics, College of Pharmacy, Seoul National University) Song, Im-Sook (Department Pharmaceutics, College of Pharmacy, Seoul National University) Chung, Suk-Jae (Department Pharmaceutics, College of Pharmacy, Seoul National University) Kim, Sang-Geon (Department of Pharmacology, College of Pharmacy, Seoul National University) Lee, Myung-Gull (Department of Pharmacology, College of Pharmacy, Seoul National University) Shim, Chang-Koo (Department Pharmaceutics, College of Pharmacy, Seoul National University)
저널정보
대한약학회 Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea 제25권 제6호
발행연도
2002.1
수록면
969 - 972 (4page)

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The alteration in the pharmacokinetic behaviors of organic cations (OCs) in rats during acute inflammation (AI) was investigated. AI was induced by an intraperitoneal injection of lipopolysaccharide (LPS, 5 mg/kg) 24 hr prior to the start of pharmacokinetic studies. Tributylmethylammonium (TBuMA) was selected as a model OC since it is largely excreted into bile, and is neither metabolized nor binds to proteins in the body. When TBuMA was administered intravenously to AI rats at a dose of 6.6 $\mu$mole/kg, the AUC was increased, while biliary excretion (i.e., cumulative amount and apparent clearance) was decreased compared to normal rats. When TBuMA was administered intravenously to AI rats at a constant rate (i.e., a bolus injection at a dose of 1.5 $\mu$mole/kg followed by a constant infusion at a rate of 1.5 $\mu$mole/kg/hr for 165 min), steady-state concentrations of plasma and liver concentrations of TBuMA were increased significantly, while in vivo hepatic uptake (amount) and canalicular excretion (clearance) were decreased. These results are consistent with a hypothesis in which both the sinusoidal uptake of TBuMA into hepatocytes via the OCT1 and the canalicular excretion of the compound from hepatocytes via the P-gp are decreased by LPS-induced AI.

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