Hepatosplanchnic haemodynamics and renal blood flow and function in rats with liver failure

Javlé, P.; Yates, J; Kynaston, Howard; Parsons, K. F.; Jenkins, S. A.

doi:10.1136/gut.43.2.272

Cited by 30 publications

(37 citation statements)

References 29 publications

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“…This results in the inhibition of transcription (Keppler et al 1974). GalN-induced liver injury has also been linked to renal failure (Javle et al 1998). Anand et al (2002) showed that treatment of D-GalN results in renal failure manifested by the decrease in renal blood flow, creatinine clearance in renal cortex.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of ellagic acid in d-galactosamine-induced kidney damage in rats

et al. 2015

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D-Galactosamine (D-GalN), which is an established experimental toxin, primarily causes liver injury by the generation of free radicals and depletion of UTP nucleotides. D-GalN intoxication also induces renal dysfunction thus, renal failure is often associated with the end-stage of the liver damage. We have investigated both preventive and curative effects of ellagic acid (EA) in this study. EA treatment at a gavage dose of 20 mg/kg body weight was administered before and after intraperitoneal (i.p.) injection of D-GalN at a dose of 750 mg/kg. Tissue and blood samples of animals were collected for morphological and biochemical evaluations. Our study results suggest that EA treatment both prior to and after the toxin administration successfully altered the toxic effects on the rats. Moreover, pre-treatment of EA was more protective than post-treatment indicated by histopathological and biochemical values. In conclusion, EA treatment both before and after D-GalN intoxication could protect kidney tissues against D-GalN induced oxidative stress.

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Section: Introductionmentioning

confidence: 99%

Protective effects of ellagic acid in d-galactosamine-induced kidney damage in rats

et al. 2015

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“…They found that rats with acute liver injury caused by galactosamine showed renal dysfunction that shared some common features with that seen in patients with hepatorenal syndrome, including decreased renal arterial blood flow, decreased GFR, and increased plasma creatinine with only minor renal histological abnormalities. Javle et al 26 also observed that acute administration of galactosamine decreased renal arterial blood flow, associated with an increase in intrarenal vascular shunts. Although the acute galactosamine model shares some similarities with patients with acute liver failure, it does differ in one important aspect, namely, urine production in this model is actually increased rather than the oliguria that usually occurs in patients with acute liver and renal failure.…”

Section: Discussionmentioning

confidence: 93%

“…13 Adenosine may also be involved in activation of the hepatorenal reflex in acute liver injury. The production of intrahepatic adenosine in acute liver injury will increase because of the increase in intrahepatic shunting that decreases the effective blood supply to hepatocytes, 26 massive inflammation [23][24][25] and the decrease in the recycling of adenosine through the adenosine kinase pathway. 34 We have recently suggested that renal function is modulated by a blood-flow-dependent hepatorenal reflex.…”

Section: Discussionmentioning

confidence: 99%

“…22 However, increased production of intrahepatic adenosine is expected in animals with acute injury, regardless of etiology, because of widespread nonspecific inflammation, local cellular edema/ischemia, [23][24][25] and a large increase in intrahepatic portal systemic shunting that decreases effective blood supply to hepatocytes. [25][26][27] Thus, the renal dysfunction associated with acute liver injury may also be related to activation of the hepatorenal reflex triggered by intrahepatic adenosine. This hypothesis was tested in a rat model of acute liver injury induced by thioacetamide.…”

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confidence: 98%

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Contribution of hepatic adenosine A1 receptors to renal dysfunction associated with acute liver injury in rats

et al. 2006

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Acute liver injury is associated with renal insufficiency, whose mechanism may be related to activation of the hepatorenal reflex. We previously showed that intrahepatic adenosine is involved in activation of the hepatorenal reflex to restrict urine production in both healthy rats and in rats with cirrhosis. The aim of the present study was to test the hypothesis that activation of intrahepatic adenosine receptors is involved in the pathogenesis of the renal insufficiency seen in acute liver injury. Acute liver injury was induced by intraperitoneal injection of thioacetamide (TAA, 500 mg/kg) in rats. The animals were instrumented 24 hours later to monitor systemic, hepatic, and renal circulation and urine production. Severe liver injury developed following TAA insult, which was associated with renal insufficiency, as demonstrated by decreased (approximately 25%) renal arterial blood flow, a lower (approximately 30%) glomerular filtration rate, and decreased urine production. Further, the increase in urine production following volume expansion challenge was inhibited. Intraportal, but not intravenous, administration of a nonselective adenosine receptor antagonist, 8-phenyltheophylline, improved urine production. To specify receptor subtype, the effects of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, an adenosine A(1) receptor antagonist) and 3,7-dimethyl-1-propargylxanthine (DMPX, an adenosine A(2) receptor antagonist) were compared. Intraportal but not intravenous administration of DPCPX greatly improved impaired renal function induced by acute liver injury, and this beneficial effect was blunted in rats with liver denervation. In contrast, neither intraportal nor intravenous administration of DMPX showed significant improvement in renal function. In conclusion, an activated hepatorenal reflex, triggered by intrahepatic adenosine A(1) receptors, contributed to the pathogenesis of the water and sodium retention associated with acute liver injury.

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“…[1][2] Further, inhibition of hepatocyte energy metabolism, with impairment of liver marker enzymes and alteration in the membrane phospholipid composition were also reported characteristics of D-GLN induced liver damage. 3 Javle and his workers 4 reported that D-GLN induced liver injury is associated with the development of renal failure. D-GLN also causes an elevation of TNFα with increased formation of reactive oxygen species (ROS) which might be circuitously a reason for cellular oxidative insult, thereby altering the antioxidant status.…”

Section: Introductionmentioning

confidence: 99%

Attenuation of Oxidative Stress and Hepatotoxicity Induced By D–Galactosamine by a Polyherbal Formulation Ambrex–in vivo and in vitro Studies

Raslin¹,

Sathiya²,

Babu³

et al. 2017

IJPER

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Objective: To evaluate the hepatoprotective effect of Ambrex, a polyherbal formulation against D-galactosamine (D-GLN) induced hepatotoxicity in Swiss albino mice as well as in Chang liver cell lines. Materials and Methods: Ambrex was orally administered for a period of 7 days at dose levels of 250 and 500 mg/kg b.wt. D-GLN (250 mg/kg b.wt, i.p) was administered 24h prior to sacrifice the animals. The protective effect of Ambrex was evaluated by measuring plasma levels of aspartate transaminase (SGOT), alanine transaminase (SGPT), alkaline phosphatase (ALP), γ-glutamyltransferase (γGT) and total bilirubin. Its effect on antioxidants such as superoxide dismutase (SOD), catalase (CAT) and reduced glutathione (GSH) and lipid peroxide(LPO) was also determined. Histopathological evaluation of liver tissues was carried out. Results: Data revealed that Ambrex was able to restore the levels of antioxidants such as SOD, Catalase, and Glutathione to near normal and reduced the elevated plasma levels of SGOT, SGPT, ALP, γ -GT and total bilirubin. It also inhibited the formation of hepatic malondialdehyde induced by D -GLN. In vitro studies revealed that Ambrex protected D-GLN induced hepatotoxicity (30µM/ ml) at dose levels of 5, 50 and 500ng/ml. Further, mRNA expression also illustrated that Ambrex inhibited the over expression of Bax, Caspase 3, TNF-α, IL-2 and CYP-450. A substantial decrease in the mRNA expression of anti-apoptotic marker Bcl2 was also observed. Conclusion: Results suggest that Ambrex has appreciable hepatoprotective effect which was evident from both in vivo and in vitro results.

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Hepatosplanchnic haemodynamics and renal blood flow and function in rats with liver failure

Cited by 30 publications

References 29 publications

Protective effects of ellagic acid in d-galactosamine-induced kidney damage in rats

Protective effects of ellagic acid in d-galactosamine-induced kidney damage in rats

Contribution of hepatic adenosine A1 receptors to renal dysfunction associated with acute liver injury in rats

Attenuation of Oxidative Stress and Hepatotoxicity Induced By D–Galactosamine by a Polyherbal Formulation Ambrex–in vivo and in vitro Studies

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