Effect of neonatal capsaicin treatment on haemodynamics and renal function in cirrhotic rats

Li, Y

doi:10.1136/gut.52.2.293

Cited by 31 publications

(23 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…All these changes are in accordance with previous reports regarding the hemodynamics and renal function in rats with hepatic failure. [27][28][29][30] Taking together, these data confirmed that we successfully established an animal model of functional renal failure in rats with FHF. To exclude effects of the systemic circulation on renal function, we simultaneously monitored SBP of animal models in order to exclude the prerenal azotemia.…”

Section: Discussionsupporting

confidence: 71%

Tumor necrosis factor-alpha-induced reduction of glomerular filtration rate in rats with fulminant hepatic failure

Wang

et al. 2014

Laboratory Investigation

View full text Add to dashboard Cite

The mechanism of renal failure during fulminant hepatic failure (FHF) or end-stage of liver disease is not fully understood. The present study aims to delineate the mechanisms of decreased glomerular filtration rate (GFR) in acute hepatic failure. A rat model of renal insufficiency in severe liver injury was established by lipopolysaccharide (LPS) plus D-galactosamine (GalN) exposure. GFR was evaluated by continuous infusion of fluorescein isothiocyanate-inulin with implanted micro-osmotic pumps. GalN/LPS intoxication resulted in severe hepatocyte toxicity as evidenced by liver histology and biochemical tests, whereas renal morphology remained normal. GFR was reduced by 33% of the controls 12 h after GalN/LPS exposure, accompanied with a decreased serum sodium levels, a marked increase in serum TNF-a and ET-1 levels as well as significantly upregulated renal type 1 inositol 1,4,5-trisphosphate receptor (IP 3 R1) expression. The upregulated IP 3 R1 expression was abrogated by the treatment of anti-TNF-a antibodies, but not by 2-aminoethoxydiphenylborate (2-APB), which blocks the inositol 1,4,5-trisphosphate signaling pathway. Treatments with either TNF-a antibodies or 2-APB also significantly improved the compromised GFR, elevated serum urea nitrogen and creatinine levels, and reversed the decrease in glomerular inulin space and the increase in glomerular calcium content in GalN/LPS-exposed rats. The extent of acute liver injury as reflected by serum ALT levels was much more attenuated by anti-TNF-a antibodies than by 2-APB. Liver histology further confirmed that anti-TNF-a antibodies conferred better protection than 2-APB in GalN/LPS-exposed rats. LPS-elicited TNF-a over-production is responsible for decreased GFR through IP 3 R1 overexpression, and the compromised GFR resulted in the development of acute renal failure in rats with FHF.

show abstract

Section: Discussionsupporting

confidence: 71%

Tumor necrosis factor-alpha-induced reduction of glomerular filtration rate in rats with fulminant hepatic failure

Wang

et al. 2014

Laboratory Investigation

View full text Add to dashboard Cite

show abstract

“…Li and colleagues demonstrated that neonatal capsaicin denervation in rats prevented the development of hyperdynamic circulation and renal dysfunction as well as ascites formation in cirrhosis. These results indicate that intact primary afferent innervation is necessary for the development of hyperdynamic circulation and ascites formation [53]. A recent study revealed reversal of the cirrhosis associated vascular dysregulation after afferent denervation in an animal model.…”

Section: Systemic and Splanchnic Circulationmentioning

confidence: 75%

Cirrhotic Ascites: Pathophysiological Changes and Clinical Implications

Bendahmash¹,

Elsiesy²,

Hamoudi³

2017

Ascites - Physiopathology, Treatment, Complications and Prognosis

View full text Add to dashboard Cite

Liver cirrhosis is associated with a wide range of systemic and pulmonary vascular abnormalities. Cardiac dysfunction also occurs in patients with advanced liver disease (cirrhotic cardiomyopathy). The circulation in cirrhosis is hyperdynamic, which is typically characterized by hypotension resulting from the associated vasodilatation and reflex tachycardia. The circulatory dysfunction in cirrhosis is the proposed pathophysiological mechanism leading to sodium and water retention in patients with liver cirrhosis. Hyperdynamic circulation is triggered by increased intrahepatic resistance due to cirrhosis, leading to a progressive increase in portal venous pressure. As portal hypertension worsens, local production of vasodilators increases due to endothelial activation, leading to splanchnic and systemic arterial vasodilation. Nitric oxide (NO) is considered one of the most important vasodilator molecules in the splanchnic and systemic circulation. The reduction in the effective arterial blood volume results in diminished renal arterial blood flow and subsequently triggers the rennin-angiotensin-aldosterone system (RAAS), antidiuretic hormones (ADHs) and sympathetic nervous system (SNS), leading to renal artery vasoconstriction. All these changes lead to sodium retention and volume expansion, manifested as ascites and peripheral edema. Furthermore, disease progression is associated with various degrees of renal dysfunction.

show abstract

“…The aforementioned capsaicin study suggests that primary afferent nerves may be the signaling pathway from the periphery to the CNS [44] . Our subsequent study showed that capsaicin-treated BDL rats improve the renal function and do not develop ascites [46] . Moreover, both BDL-cirrhotic and portal hypertensive rats show diminished Fos expression in NTS after capsaicininduced denervation of the afferent nerves as neonates [46] .…”

Section: Central Neural Mechanismsmentioning

confidence: 82%

“…Our subsequent study showed that capsaicin-treated BDL rats improve the renal function and do not develop ascites [46] . Moreover, both BDL-cirrhotic and portal hypertensive rats show diminished Fos expression in NTS after capsaicininduced denervation of the afferent nerves as neonates [46] . These observations indicate that intact primary afferent innervation is necessary for the central neuronal activation and development or maintenance of hyperdynamic circulation.…”

Section: Central Neural Mechanismsmentioning

confidence: 82%

Cardiac and vascular changes in cirrhosis: Pathogenic mechanisms

Liu

Gaskari²,

Lee

2006

WJG

130

View full text Add to dashboard Cite

Cardiovascular abnormalities accompany both portal hypertension and cirrhosis. These consist of hyperdynamic circulation, defined as reduced mean arterial pressure and systemic vascular resistance, and increased cardiac output. Despite the baseline increased cardiac output, ventricular inotropic and chronotropic responses to stimuli are blunted, a condition known as cirrhotic cardiomyopathy. Both conditions may play an initiating or aggravating pathogenic role in many of the complications of liver failure or portal hypertension including ascites, variceal bleeding, hepatorenal syndrome and increased postoperative mortality after major surgery or liver transplantation. This review briefly examines the major mechanisms that may underlie these cardiovascular abnormalities, concentrating on nitric oxide, endogenous cannabinoids, central neural activation and adrenergic receptor changes. Future work should address the complex interrelationships between these systems.

show abstract

Effect of neonatal capsaicin treatment on haemodynamics and renal function in cirrhotic rats

Cited by 31 publications

References 45 publications

Tumor necrosis factor-alpha-induced reduction of glomerular filtration rate in rats with fulminant hepatic failure

Tumor necrosis factor-alpha-induced reduction of glomerular filtration rate in rats with fulminant hepatic failure

Cirrhotic Ascites: Pathophysiological Changes and Clinical Implications

Cardiac and vascular changes in cirrhosis: Pathogenic mechanisms

Contact Info

Product

Resources

About