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Pagina 1 a partire dal 255 risultati
Roles of changes in active glutamine transport in brain edema development during hepatic encephalopathy: an emerging concept.
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Excessive glutamine (Gln) synthesis in ammonia-overloaded astrocytes contributes to astrocytic swelling and brain edema, the major complication of hepatic encephalopathy (HE). Much of the newly formed Gln is believed to enter mitochondria, where it is recycled to ammonia, which causes mitochondrial
Pathogenesis of hepatic encephalopathy and brain edema in acute liver failure: role of glutamine redefined.
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Acute liver failure (ALF) is characterized neuropathologically by cytotoxic brain edema and biochemically by increased brain ammonia and its detoxification product, glutamine. The osmotic actions of increased glutamine synthesis in astrocytes are considered to be causally related to brain edema and
Preconditioning with L-alanyl-glutamine upon cerebral edema and hypocampus red neurons counting in rats subjected to brain ischemia/reperfusion injury.
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OBJECTIVE
To evaluate the effects of the dipeptide L-alanyl-glutamine (L-Ala-Gln) as a preconditioning agent to potentially promote reduction in the intensity of lesion or induction of resilience in rats subjected to global cerebral ischemia/reperfusion (I/R) injury.
METHODS
Thirty-six male Wistar
Glutamine, myo-inositol, and organic brain osmolytes after portocaval anastomosis in the rat: implications for ammonia-induced brain edema.
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Brain myo-inositol, an organic osmolyte, is decreased in cirrhotic patients with hepatic encephalopathy but appears unchanged in fulminant hepatic failure. An osmoregulatory response to the increase in brain glutamine may explain the decrease in brain myo-inositol; if this is the case, organic
Inhibition of brain glutamine accumulation prevents cerebral edema in hyperammonemic rats.
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The mechanism of brain swelling during hyperammonemia is not understood, but glutamine accumulation is consistently observed. We tested the hypothesis that brain swelling associated with hyperammonemia is a consequence of the osmotic effect of intracellular glutamine accumulation in brain. Increases
Arginase deficiency with lethal neonatal expression: evidence for the glutamine hypothesis of cerebral edema.
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We describe a rare and lethal case of arginase deficiency in a 2-day-old female infant with encephalopathy and cerebral edema. The levels of glutamine and arginine but not ammonia were markedly elevated, lending support to the "glutamine hypothesis" as the mechanism of cerebral edema in urea cycle
Glutamine, myo-inositol, and brain edema in acute liver failure.
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Glucose-derived osmolytes and energy impairment in brain edema accompanying liver failure: the role of glutamine reevaluated.
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Glutamine in the pathogenesis of acute hepatic encephalopathy.
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Hepatic encephalopathy (HE) is the major neurological disorder associated with liver disease. It presents in chronic and acute forms, and astrocytes are the major neural cells involved. While the principal etiological factor in the pathogenesis of HE is increased levels of blood and brain ammonia,
Effect of glutamine synthesis inhibition with methionine sulfoximine on the nitric oxide-cyclic GMP pathway in the rat striatum treated acutely with ammonia: a microdialysis study.
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Ammonia neurotoxicity is associated with overactivation of N-methyl-D-aspartate (NMDA) receptors leading to enhanced nitric oxide and cyclic GMP synthesis and to accumulation of reactive oxygen and nitrogen species. Ammonia is detoxified in the brain via synthesis of glutamine, which if accumulated
Diffusion tensor imaging supports the cytotoxic origin of brain edema in a rat model of acute liver failure.
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OBJECTIVE
Brain edema is a severe complication of acute liver failure (ALF) that has been related to ammonia concentrations. Two mechanisms have been proposed in the pathogenesis: vasogenic edema that is secondary to the breakdown of the blood-brain barrier and cytotoxic edema caused by ammonia
Cerebral edema and liver disease: classic perspectives and contemporary hypotheses on mechanism.
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Liver disease is a growing public health concern. Hepatic encephalopathy, the syndrome of brain dysfunction secondary to liver disease, is a frequent complication of both acute and chronic liver disease and cerebral edema (CE) is a key feature. While altered ammonia metabolism is a key contributor
Mechanisms of brain edema in acute liver failure and impact of novel therapeutic interventions.
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Continued elucidation of the mechanisms of brain edema in acute liver failure (ALF) has established ammonia and the astrocyte as major players in its pathogenesis. The metabolism of ammonia to glutamine appears to be a requisite, and is followed by an osmotic disturbance in the brain, mitochondrial
Blood-brain barrier water permeability and brain osmolyte content during edema development.
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OBJECTIVE
To determine mechanisms that limit changes in brain water content during acute edema development.
METHODS
A controlled, laboratory investigation of the physiologic and biochemical correlates of osmotic edema was performed in rats. Hypoosmotic hyponatremia was induced by intraperitoneal
Brain osmolyte content and blood-brain barrier water permeability surface area product in osmotic edema.
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Brain edema was induced in adult rats by intraperitoneal injection of distilled water equivalent to 15% of the animal's body weight. Mean +/- SEM serum osmolality fell from 291 +/- 3 mOsm to 253 +/- 4 mOsm during the next hour while cerebral gray matter water content increased from 79.5 +/- 0.2% to
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