Pharmacokinetics of cefpiramide in rats acutely intoxicated with carbon tetrachloride.

Chu, Li; Nakayama, Shuko; Kurosaki, Yuji; Nakayama, Tomohiro; Kimura, Takeshi

doi:10.1248/bpb1978.13.186

Cited by 7 publications

(4 citation statements)

References 14 publications

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“…Acute hepatic failure induced experimentally with CCl 4 in animals is accompanied by a reduction in the renal tubular secretion of cefpiramine and impaired intestinal sugar transport, in addition to the suppression of various hepatic functions (Li et al 1990 ;Sugihara et al 1992 ;Castilla-Cortazar et al 1997). Acute renal failure induced by glycerol or uranyl nitrate also reduces the hepato-biliary transport of certain drugs, modulates the distribution of drugs into the central nervous system and decreases the activity of various hepatic microsomal enzymes (Bowmer & Yates 1984 ;Naora et al 1999).…”

Section: Introductionmentioning

confidence: 99%

Expression and function of P-glycoprotein in rats with carbon tetrachloride-induced acute hepatic failure

Huang

Murakami

Okochi

et al. 2001

Journal of Pharmacy and Pharmacology

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Acute hepatic failure was induced experimentally in rats by intraperitoneal injection of 2.5 mL kg(-1) carbon tetrachloride (CCl4), and the effects on the expression and function of P-glycoprotein in the liver, kidney and brain were evaluated. The CCl4 injection significantly increased the indicators of hepatic function (glutamate oxaloacetate transaminase, glutamate pyruvate transaminase), but not of renal function (blood urea nitrogen, glomerular filtration rate). In rats with acute hepatic failure, the hepatic P-glycoprotein concentration increased 1.5-fold and the ATP concentration decreased to approximately 40% that in control rats. In contrast, P-glycoprotein concentrations in the kidney and brain and ATP concentrations in the kidney remained unchanged. The in-vivo P-glycoprotein function in these tissues was suppressed as evaluated by biliary and renal secretory clearances and brain distribution of rhodamine 123, a P-glycoprotein substrate. These findings suggest that factors other than P-glycoprotein concentration are involved in the systemic suppression of P-glycoprotein function in diseased rats. In Caco-2 cells, plasma collected from CCl4-treated rats exhibited a greater inhibitory effect on P-glycoprotein-mediated transport of rhodamine 123 than that from control rats, suggesting the accumulation of an endogenous P-glycoprotein substrate/inhibitor in the plasma of diseased rats. In fact, the plasma concentration of corticosterone, an endogenous P-glycoprotein substrate, increased 2-fold in CCl4-treated rats compared with control rats. It was demonstrated that P-glycoprotein function is systemically suppressed in rats with CCl4-induced acute hepatic failure, not only in the target organ (liver), but also in other organs (kidney and brain), although the P-glycoprotein concentration remained unchanged in the kidney and brain, and increased in the liver. In the systemic suppression of the P-glycoprotein function in the diseased state, the alteration of plasma concentrations or components of endogenous P-glycoprotein-related compounds, such as corticosterone, would likely be involved.

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Section: Introductionmentioning

confidence: 99%

Expression and function of P-glycoprotein in rats with carbon tetrachloride-induced acute hepatic failure

Huang

Murakami

Okochi

et al. 2001

Journal of Pharmacy and Pharmacology

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“…Several studies indicated that the mRNA expression of hepatic CYP450 and transporters, such as CYP2C11, CYP2E1, CYP3A2, CYP1A2, Ntcp, Oct1, Oatp2, Mrp2, and Bsep, were significantly decreased, while Mrp3, Mrp4, and Mdr1 were increased by CCl 4 treatment (Yokogawa et al 2004;. Acute hepatic failure caused by administration of CCl 4 in animals is also accompanied by a reduction in renal tubular secretion and impaired intestinal sugar transport, in addition to the suppression of various hepatic functions (Li et al 1990;Sugihara et al 1992;Castilla et al 1997).…”

Section: Introductionmentioning

confidence: 99%

Pharmacokinetics of bicyclol in rats with acute hepatic failure

et al. 2008

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The aim of present study is to evaluate the pharmacokinetics of bicyclol in carbon tetrachloride (CCl(4))-intoxicated rats. The plasma concentration of bicyclol was detected in rats after a single oral or intravenous administration by high-performance liquid chromatography (HPLC) analysis. Rat intestinal and hepatic perfusion models were employed to clarify the respective effect of gut and liver on the pharmacokinetics of bicyclol in acute hepatic failure (AHF) rats. Rat in vitro microsomal incubation was also conducted. The bioavailability of bicyclol was increased 3.1-fold after CCl(4) intoxication in rats. The area under the curve (AUC)((0-infinity)), C(max), and clearance (CL) of bicyclol after intravenous administration were 13.4 mg h l(-1), 18.8 mg l(-1), and 1.8 l h(-1) kg(-1) in control rats, and 130 mg h l(-1), 33.1 mg l(-1), and 0.15 l h(-1) kg(-1) in AHF rats, respectively. In the present study we investigated the pharmacokinetics of bicyclol in CCl(4)-intoxicated rats and differentiated the respective role of intestine and liver by using in situ intestinal and hepatic perfusion in rats, and in vitro rat microsomes incubation. The studies are expected to provide a better understanding related to the alteration of pharmacokinetics of bicyclol in pathological situation.

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“…6) Acute hepatic failure in animals is accompanied by a reduction in the renal tubular secretion and impaired intestinal sugar transport, in addition to the suppression of various hepatic functions. [7][8][9] In the present study, we investigated the eŠects of renal or hepatic failure on the intestinal absorption of tacrolimus using the simultaneous perfusion techniques in rat intestine. These studies in rats are expected to provide a better understanding of the relationship between the disease states and the absorption of tacrolimus.…”

Section: Introductionmentioning

confidence: 99%

Effect of Experimental Acute Renal and Hepatic Failure on Absorption of Tacrolimus in Rat Small Intestine

Tamura¹,

Ohike²,

Tokunaga³

et al. 2004

Drug Metabolism and Pharmacokinetics

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The objective of this study is to evaluate the effect of acute renal or hepatic failure on the intestinal absorption of tacrolimus. Simultaneous perfusion study in rat small intestine revealed that the extent of absorption into blood vessels was decreased in the jejunum and the ileum of rat of acute renal failure due to the decrease in the uptake of tacrolimus into enterocytes. In contrast, there observed no significant changes in tacrolimus absorption in rat of acute hepatic failure. Since it has been reported that tacrolimus absorption is regulated mainly by Cytochrome P-450 (CYP) mediated metabolism in the jejunum, but by P-glycoprotein (P-gp) mediated efflux in the ileum, these factors might contribute to the changes in intestinal absorption of tacrolimus in rat of acute renal failure. Enzyme inhibitor, ketoconazole, was co-perfused with tacrolimus to specify the effect of CYP and P-gp. However, since ketoconazole failed to recover the permeability in the jejunum and ileum of rat of acute renal failure, it is considered that the changes in CYP or P-gp functions might not be involved in the decreased uptake of tacrolimus. This type of kinetic study in rats should be valuable to identify the precise mechanisms of drug absorption and the effects of various diseases on it, such as acute renal or hepatic failure.

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Pharmacokinetics of cefpiramide in rats acutely intoxicated with carbon tetrachloride.

Cited by 7 publications

References 14 publications

Expression and function of P-glycoprotein in rats with carbon tetrachloride-induced acute hepatic failure

Expression and function of P-glycoprotein in rats with carbon tetrachloride-induced acute hepatic failure

Pharmacokinetics of bicyclol in rats with acute hepatic failure

Effect of Experimental Acute Renal and Hepatic Failure on Absorption of Tacrolimus in Rat Small Intestine

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