scholarly journals NMR study of 13C-glucose and 13C-acetate metabolism in the brain of rats with acute liver failure

2008 ◽  
Vol 81 ◽  
pp. 9-13
Author(s):  
C. Zwingmann ◽  
N. Chatauret ◽  
D. Leibfritz ◽  
R. F. Butterworth
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Acetate Metabolism ◽  
Nmr Study ◽  
The Brain

scholarly journals Wilson Disease-Induced Acute Liver Failure (NWI = 13) Salvaged without Liver Transplant by Plasmapheresis

2021 ◽  
Vol 11 (01) ◽  
pp. e145-e147
Author(s):  
Nida Mirza ◽  
Ravi Bharadwaj ◽  
Smita Malhotra ◽  
Anupam Sibal
Keyword(s):  
Liver Transplantation ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Wilson Disease ◽  
Prognostic Score ◽  
Prognostic Index ◽  
Kidney Injury ◽  
Copper Metabolism ◽  
Life Saving ◽  
The Brain

AbstractWilson disease (WD) is a disorder of copper metabolism resulting in accumulation of copper in vital organs of the human body, predominantly in the liver and the brain. Acute liver failure in WD has a bad prognosis, especially with a score ≥11 in the revised WD prognostic index; emergency liver transplantation is considered the only life-saving option in this scenario. Here, we reported a girl patient with WD-induced liver failure and poor prognostic score who was rescued by plasmapheresis. She also manifested severe Coombs negative hemolytic anemia and acute kidney injury. This case report highlights the utility of an adjunctive modality besides liver transplantation for the management of fulminant liver failure caused by WD.

scholarly journals Glutamine synthetase expression in the brain during experimental acute liver failure (immunohistochemical study)

2021 ◽  
Vol 11 (10) ◽  
pp. 342-356
Author(s):  
T. Shulyatnikova ◽  
V. Tumanskiy
Keyword(s):  
White Matter ◽  
Glutamine Synthetase ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Caudate Nucleus ◽  
Immunohistochemical Study ◽  
Clinical Signs ◽  
Brain Regions ◽  
Progressive Increase ◽  
The Brain

The aim of the study was to determine the immunohistochemical level of glutamine synthetase (GS) expression in different brain regions in the conditions of experimental acute liver failure in rats. Materials and methods. The study was conducted in Wistar rats: 5 sham (control) animals and 10 rats with acetaminophen induced liver failure model (AILF). The immunohistochemical study of GS expression in the sensorimotor cortex, white matter, hippocampus, thalamus, caudate nucleus/putamen was carried out in the period of 12-24 h after acetaminophen treatment. Results. Beginning from the 6th hour after acetaminophen treatment all AILF-animals showed the progressive increase in clinical signs of acute brain disfunction finished in 6 rats by comatose state up to 24 h - they constituted subgroup AILF-B, “non-survived”. 4 animals survived until the 24 h - subgroup AILF-A, “survived”. In the AILF-B group, starting from 16 to 24 hours after treatment, a significant (relative to control) regionally-specific dynamic increase in the level of GS expression was observed in the brain: in the cortex – by 307.33 %, in the thalamus – by 249.47%, in the hippocampus – by 245.53%, in the subcortical white matter – by 126.08%, from 12th hour – in the caudate nucleus/putamen, by 191.66 %; with the most substantive elevation of GS expression in the cortex: by 4.07 times. Conclusion. Starting from the 16th hours after the acetaminophen treatment (from the 12th h in the caudate nucleus/putamen region) and up to 24 h, it is observed reliable compared to control dynamic increase in GS protein expression in the cortex, white matter, hippocampus, thalamus, caudate nucleus/putamen of the rat brain with the most significant elevation in the cortex among other regions. The heterogeneity in the degree of GS expression rising in different brain regions potentially may indicate regions more permeable for ammonia and/or other systemic toxic factors as well as heterogeneous sensitivity of brain regions to deleterious agents in conditions of AILF. Subsequently, revealed diversity in the GS expression reflects the specificity of reactive response of local astroglia in the condition of AILF-encephalopathy during specific time-period. The dynamic increase in the GS expression associated with impairment of animal state, indicates involvement of increased GS levels in the mechanisms of experimental acute hepatic encephalopathy.

scholarly journals S-Adenosylmethionine Deficiency and Brain Accumulation of S-Adenosylhomocysteine in Thioacetamide-Induced Acute Liver Failure

Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 2135
Author(s):  
Anna Maria Czarnecka ◽  
Wojciech Hilgier ◽  
Magdalena Zielińska
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Redox Homeostasis ◽  
Cerebral Function ◽  
Total Glutathione ◽  
Cellular Redox ◽  
Therapeutic Value ◽  
Transsulfuration Pathway ◽  
Subsequent Hydrolysis ◽  
The Brain

Background: Acute liver failure (ALF) impairs cerebral function and induces hepatic encephalopathy (HE) due to the accumulation of neurotoxic and neuroactive substances in the brain. Cerebral oxidative stress (OS), under control of the glutathione-based defense system, contributes to the HE pathogenesis. Glutathione synthesis is regulated by cysteine synthesized from homocysteine via the transsulfuration pathway present in the brain. The transsulfuration-transmethylation interdependence is controlled by a methyl group donor, S-adenosylmethionine (AdoMet) conversion to S-adenosylhomocysteine (AdoHcy), whose removal by subsequent hydrolysis to homocysteine counteract AdoHcy accumulation-induced OS and excitotoxicity. Methods: Rats received three consecutive intraperitoneal injections of thioacetamide (TAA) at 24 h intervals. We measured AdoMet and AdoHcy concentrations by HPLC-FD, glutathione (GSH/GSSG) ratio (Quantification kit). Results: AdoMet/AdoHcy ratio was reduced in the brain but not in the liver. The total glutathione level and GSH/GSSG ratio, decreased in TAA rats, were restored by AdoMet treatment. Conclusion: Data indicate that disturbance of redox homeostasis caused by AdoHcy in the TAA rat brain may represent a deleterious mechanism of brain damage in HE. The correction of the GSH/GSSG ratio following AdoMet administration indicates its therapeutic value in maintaining cellular redox potential in the cerebral cortex of ALF rats.

scholarly journals Quantitative multivoxel 1H MR spectroscopy of the brain in children with acute liver failure

2008 ◽  
Vol 18 (11) ◽  
pp. 2601-2609 ◽  
Author(s):  
Paul E. Sijens ◽  
Heyder Alkefaji ◽  
Roelineke J. Lunsing ◽  
Francjan J. van Spronsen ◽  
Linda C. Meiners ◽  
...  
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Mr Spectroscopy ◽  
1H Mr Spectroscopy ◽  
The Brain

Subchronic treatment with acai frozen pulp prevents the brain oxidative damage in rats with acute liver failure

2016 ◽  
Vol 31 (6) ◽  
pp. 1427-1434 ◽  
Author(s):  
Fernanda de Souza Machado ◽  
Jonnsin Kuo ◽  
Mariane Farias Wohlenberg ◽  
Marina da Rocha Frusciante ◽  
Márcia Freitas ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Subchronic Treatment ◽  
The Brain

The Na–K–Cl cotransporter in the brain edema of acute liver failure

2011 ◽  
Vol 54 (2) ◽  
pp. 272-278 ◽  
Author(s):  
Arumugam R. Jayakumar ◽  
Vanessa Valdes ◽  
Michael D. Norenberg
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Brain Edema ◽  
The Brain

scholarly journals The Status of Bile Acids and Farnesoid X Receptor in Brain and Liver of Rats with Thioacetamide-Induced Acute Liver Failure

2020 ◽  
Vol 21 (20) ◽  
pp. 7750
Author(s):  
Anna Maria Czarnecka ◽  
Krzysztof Milewski ◽  
Jan Albrecht ◽  
Magdalena Zielińska
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Bile Acids ◽  
Tissue Expression ◽  
Farnesoid X Receptor ◽  
Mrna Levels ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
The Status ◽  
The Brain

Acute liver failure (ALF) leads to neurological symptoms defined as hepatic encephalopathy (HE). Although accumulation of ammonia and neuroinflammation are generally accepted as main contributors to HE pathomechanism, a buildup of bile acids (BA) in the blood is a frequent component of liver injury in HE patients. Recent studies have identified the nuclear farnesoid X receptor (FXR) acting via small heterodimer partner (SHP) as a mediator of BA-induced effects in the brain of ALF animals. The present study investigated the status of the BA–FXR axis in the brain and the liver, including selective changes in pertinent genes in thioacetamide (TAA)-induced ALF in Sprague–Dawley rats. FXR was found in rat neurons, confirming earlier reports for mouse and human brain. BA accumulated in blood but not in the brain tissue. Expression of mRNAs coding for Fxr and Shp was reduced in the hippocampus and of Fxr mRNA also in the cerebellum. Changes in Fxr mRNA levels were not followed by changes in FXR protein. The results leave open the possibility that mobilization of the BA–FXR axis in the brain may not be necessarily pathognomonic to HE but may depend upon ALF-related confounding factors.

The brain in acute liver failure. A tortuous path from hyperammonemia to cerebral edema

2008 ◽  
Vol 24 (1) ◽  
pp. 5-14 ◽  
Author(s):  
Peter Nissen Bjerring ◽  
Martin Eefsen ◽  
Bent Adel Hansen ◽  
Fin Stolze Larsen
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Cerebral Edema ◽  
The Brain

Magnetic resonance of the brain in chronic and acute liver failure

2013 ◽  
Vol 29 (4) ◽  
pp. 937-944 ◽  
Author(s):  
Laia Chavarria ◽  
Juan Cordoba
Keyword(s):  
Magnetic Resonance ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
The Brain

Real-time assessment of13C metabolism reveals an early lactate increase in the brain of rats with acute liver failure

2014 ◽  
pp. n/a-n/a ◽  
Author(s):  
Laia Chavarria ◽  
Jordi Romero-Giménez ◽  
Eva Monteagudo ◽  
Silvia Lope-Piedrafita ◽  
Juan Cordoba
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Real Time ◽  
The Brain ◽  
Time Assessment
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