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galactosamine/ødem
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The appearance of D-galactosamine-induced hepatitis and generalized edema in adrenalectomized rats.
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In adrenalectomized female rats a single dose of 375 mg D-galactosamine.HCl per kg of body weight produces both hepatitis and generalized edema with ascites. These alterations depend upon the dose and the time interval after injection of the aminosugar. The effect is specific for D-galactosamine;
Brain edema in rabbits with galactosamine-induced fulminant hepatitis. Regional differences and effects on intracranial pressure.
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Brain edema and intracranial hypertension are major complications of fulminant hepatic failure. We investigated the development of brain edema and monitored intracranial pressure in rabbits with toxic hepatitis induced by galactosamine. Using a gravimetric technique to assay small tissue samples, we
Hemodynamic, biochemical and morphological changes in the dextran and D-galactosamine-induced edemas in rats.
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Dextran (600 mg/kg i.p.) and D-galactosamine (300 mg/kg s.c.)-induced edemas in the rat have been evaluated and compared on the basis of hemodynamic, biochemical and morphological investigations. The genesis of the edema induced by dextran was quicker (1-3 hr) than that induced by D-galactosamine.
Effects of prostaglandin E2 on brain edema and liver histopathology in a galactosamine-induced fulminant hepatic failure rat model.
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The effects of prostaglandin E2 (PGE2) on the histopathology of liver and brain edema was studied in the galactosamine-induced fulminant hepatic failure (Ga1N-FHF) rat model. The effect of PGE2 on the development of brain edema was studied in grade II coma FHF rats by electron microscopy and by
Electron microscopic evaluation of brain edema in rabbits with galactosamine-induced fulminant hepatic failure: ultrastructure and integrity of the blood-brain barrier.
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Brain edema is a major complication of fulminant hepatic failure and is responsible for death in a large percentage of patients. We previously demonstrated the progressive accumulation of water in grey matter areas of the brain in the rabbit with galactosamine-induced fulminant hepatic failure. We
Regional cerebral edema and chloride space in galactosamine-induced liver failure in rats.
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The pathogenesis of cerebral edema, which is a major complication of fulminant hepatic failure, is poorly understood. In previous studies, increased regional brain water content was observed in rats at an early stage of acute liver failure caused by galactosamine. At a later stage when the animals
Brain edema and the blood brain barrier in galactosamine-induced fulminant hepatic failure rats. An animal model for evaluation of liver support systems.
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Rats with galactosamine-induced fulminant hepatic failure (FHF) have been a popular animal model for the evaluation of liver support systems. Because development of brain edema is a major and frequent complication during FHF, it was studied for this report. The degree of hepatocyte necrosis closely
Inhibition of galactosamine induced edemas in the rat by drugs preventing macromolecular leakage from the hamster cheek pouch microvasculature.
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We have shown that terbutaline and dimethpyrindene, 2 drugs which prevent macromolecular leakage in the in vivo--bio-assay of Hamster Cheek Pouch, either by direct action onendothelial cells or by blocking histamine receptors at the microvascular leakage sites, can also prevent macromolecular
Cerebral edema in the rat with galactosamine induced severe hepatitis.
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With D-galactosamine hydrochloride severe hepatitis was induced in rats and the water content of cerebrum, cerebellum and brain stem determined. The animals showed a parallel increase in cerebral water content and occurrence of cerebral symptoms.
Mannitol treatment of cerebral edema in rats with galactosamine-induced severe hepatitis.
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Induction of edema in the adrenalectomized rat by D-galactosamine.
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Brain edema in acute liver failure. Insight from experimental studies.
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Brain edema is a leading cause of death in fulminant hepatic failure (FHP). Animal studies are needed to gain further insight into its pathogenesis. The authors describe and analyze the results of brain studies in two animal models of FHF, the rabbit with galactosamine induced hepatitis and the
Brain edema in acute liver failure: role of neurosteroids.
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Brain edema is a major neurological complication of acute liver failure (ALF) and swelling of astrocytes (cytotoxic brain edema) is the most prominent neuropathological abnormality in this condition. Elevated brain ammonia level has been strongly implicated as an important factor in the mechanism of
Effects of D-galactosamine-induced acute liver injury on mortality and pulmonary responses to Escherichia coli lipopolysaccharide. Modulation by arachidonic acid metabolites.
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Multiple extrapulmonary organ system failures increase mortality, permeability edema, and alveolar inflammation during gram-negative sepsis because of abnormal regulation of host inflammatory responses. We tested the hypothesis that acute hepatocytic injury induced by the selective hepatotoxin,
[Protective effect of the histone deacetylase inhibitor ACY1215 against brain edema in mice with acute liver failure].
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Objective: To investigate the protective effect of ACY1215 (Rocilinostat), a histone deacetylase inhibitor, against brain edema in mice with acute liver failure. Methods: Lipopolysaccharide combined with D-galactosamine was used to establish a mouse model of acute liver failure, and ACY1215 was used
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