Restrictive model of compensated carbon tetrachloride-induced cirrhosis in rats

Régimbeau, Jean‐Marc; Fuks, David; Kohneh-Shahri, N.; Terris, Benoı̂t; Soubrane, Olivier

doi:10.3748/wjg.14.6943

Cited by 12 publications

(17 citation statements)

References 24 publications

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“…Many different experimental HRS models were used in experimental studies; these included models of toxic liver injury induced by CCl 4 , ligation of bile tract, partial ligation of portal vein, and partial hepatectomy and galactosamine-intoxicated experimental animals [ 24 – 27 ]. Some of these were chronic HRS models in which liver failure and consequent renal failure develop within a few weeks or months.…”

Section: Discussionmentioning

confidence: 99%

Effect of Nitric Oxide Pathway Regulation on Water/Sodium Balance and Renal Function in a Rodent Model of Acute Liver and Renal Failure

et al. 2014

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BackgroundThe pathomechanism of acute hepatorenal syndrome (HRS), a particular form of acute renal failure that occurs in the course of acute liver injury, is still poorly understood. The aim of our study was to estimate the influence of the activation and inhibition of the nitric oxide pathway on the water/sodium balance and development of acute renal failure in the course of HRS.Material/MethodsWe used male Sprague-Dawley rats in the acute galactosamine (Ga1N) model of HRS. The nitric oxide synthase (NOS) inhibitors L-NAME and L-arginine were administered intraperitoneally before and after liver damage.ResultsHRS developed in all tested groups. L-NAME increased osmotic clearance and urine volume more effectively before liver injury. Furthermore, administration of L-NAME increased creatinine clearance both before and after Ga1N injection. A double dose of L-NAME did not yield further improvement before Ga1N injection, but improved creatinine clearance after Ga1N intoxication. Injection of L-arginine increased sodium excretion and urine volume, but only after liver injury. Moreover, L-arginine injected after Ga1N caused significant improvement of the creatinine clearance in a dose-dependent manner.ConclusionsOur study shows that inhibition of the nitric oxide pathway improves parameters of water and sodium balance and prevents development of acute renal failure in the course of acute liver injury and liver failure. Activation of the nitric oxide system also has a favorable influence on water/sodium balance and renal failure, but only after liver injury.

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Section: Discussionmentioning

confidence: 99%

Effect of Nitric Oxide Pathway Regulation on Water/Sodium Balance and Renal Function in a Rodent Model of Acute Liver and Renal Failure

et al. 2014

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“…), and the eventual use of phenobarbitone in the drinking water as enzyme inducer. 11 In addition to these parameters, the susceptibility of a given animal strain, depending on immunologic background, affects efficiency and severity of liver fibrosis development. 12 – 14 The impact of immune status is illustrated by variation in the severity of fibrosis following CCl 4 administration observed (i) in Balbc and C57BL/6 mice due to a different Th1/Th2 cytokines response 13 and (ii) in wild-type Balbc mice, severe combined immunodeficiency (SCID) mice (lacking B, T cells but having NK cells), and SCID beige (lacking B, T and NK cells) mice.…”

Section: Animal Models Of Liver Diseasesmentioning

confidence: 99%

Animal Models for Fibrotic Liver Diseases: What We Have, What We Need, and What Is under Development

Delire

Stärkel

Leclercq

2015

JCTH

139

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Liver fibrosis is part of the wound-healing response to liver damage of various origins and represents a major health problem. Although our understanding of the pathogenesis of liver fibrosis has grown considerably over the last 20 years, effective antifibrotic therapies are still lacking. The use of animal models is crucial for determining mechanisms underlying initiation, progression, and resolution of fibrosis and for developing novel therapies. To date, no animal model can recapitulate all the hepatic and extra-hepatic features of liver disease. In this review, we will discuss the current rodent models of liver injuries. We will then focus on the available ways to target specifically particular compounds of fibrogenesis and on the new models of liver diseases like the humanized liver mouse model.

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“…Attempts to overcome these pitfalls include the use of cytochrome P450 inducers (e.g. phenobarbital in the drinking water) 8 , the individualization of CCl4 doses according to the body weight or to the changes in body weight of the animal 7 , 9 , and diverse duration and schedules of CCl4 administration such as once 6 , 7 , twice 10 or thrice 11 , 12 a week or others 9 , 13 . Such variety of protocols reflect that the prior problems are still present.…”

Section: Introductionmentioning

confidence: 99%

Comparison of Two Protocols of Carbon Tetrachloride-Induced Cirrhosis in Rats – Improving Yield and Reproducibility

Fortea

Fernández-Mena

Puerto

et al. 2018

Sci Rep

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Despite being a cardinal experimental model, the induction of cirrhosis in rats by repeated exposure to carbon tetrachloride (CCl4) has low reproducibility. Here, we compared two models of cirrhosis induced by orogastric administration of CCl4 once (CCl4-1xWk) or twice a week (CCl4-2xWk) for 12 weeks in male Sprague-Dawley rats. Control rats received water instead of CCl4. Both CCl4 protocols similarly attenuated body weight gain (p < 0.01 vs. Control). Although both CCl4 protocols increased hepatic fibrosis, portal hypertension and splenomegaly, the magnitude of these alterations was higher and more consistent in CCl4-2xWk rats. Importantly, two CCl4-1xWk rats did not develop cirrhosis versus a 100% yield of cirrhosis in CCl4-2xWk rats. The CCl4-2xWk protocol consistently induced liver atrophy together with hematological, biochemical and coagulation abnormalities characteristic of advanced cirrhosis that were absent in CCl4-1xWk rats. Ascites occurred in 20% and 80% of rats in theCCl4-1xWk and CCl4-2xWk groups (p < 0.01). All rats showed normal renal function, arterial blood gases and stable systemic hemodynamics. The total dose of CCl4 and mortality rate were similar in both protocols. The CCl4-2xWk protocol, therefore, was highly reproducible and effective for the induction of experimental cirrhosis within a confined time, representing a valuable advance for liver research.

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Restrictive model of compensated carbon tetrachloride-induced cirrhosis in rats

Cited by 12 publications

References 24 publications

Effect of Nitric Oxide Pathway Regulation on Water/Sodium Balance and Renal Function in a Rodent Model of Acute Liver and Renal Failure

Effect of Nitric Oxide Pathway Regulation on Water/Sodium Balance and Renal Function in a Rodent Model of Acute Liver and Renal Failure

Animal Models for Fibrotic Liver Diseases: What We Have, What We Need, and What Is under Development

Comparison of Two Protocols of Carbon Tetrachloride-Induced Cirrhosis in Rats – Improving Yield and Reproducibility

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