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Increased toll-like receptor 4 in cerebral endothelial cells contributes to the astrocyte swelling and brain edema in acute hepatic encephalopathy.

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Astrocyte swelling and the subsequent increase in intracranial pressure and brain herniation are major clinical consequences in patients with acute hepatic encephalopathy. We recently reported that conditioned media from brain endothelial cells (ECs) exposed to ammonia, a mixture of cytokines (CKs)

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

Brain edema dynamics in patients with overt hepatic encephalopathy A magnetic resonance imaging study.

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The aim of our study was to investigate the dynamics of brain water content assessed by magnetic resonance imaging (MRI) applications in patients with cirrhosis and overt episodic hepatic encephalopathy (HE). METHODS Twenty-four patients with cirrhosis and overt HE, 9 healthy controls and 9 controls

Xiaochaihutang Improves the Cortical Astrocyte Edema in Thioacetamide-Induced Rat Acute Hepatic Encephalopathy by Activating NRF2 Pathway.

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Oxidative stress induced by high ammonia, which leads to astrocyte edema, is the key to acute hepatic encephalopathy (AHE). Nuclear factor erythroid 2-related factor 2 (NRF2) has been implicated in oxidative stress, but the mechanism of NRF2 against ammonia-induced astrocytes edema has not been

Role of cerebral endothelial cells in the astrocyte swelling and brain edema associated with acute hepatic encephalopathy.

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Brain edema is an important complication of acute hepatic encephalopathy (AHE), and astrocyte swelling is largely responsible for its development. Elevated blood and brain ammonia levels have been considered as major etiological factors in this edema. In addition to ammonia, recent studies have

Brain edema and inflammatory activation in bile duct ligated rats with diet-induced hyperammonemia: A model of hepatic encephalopathy in cirrhosis.

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Studies of the pathogenesis of hepatic encephalopathy are hampered by the lack of a satisfactory animal model. We examined the neurological features of rats after bile duct ligation fed a hyperammonemic diet (BDL+HD). Six groups were studied: sham, sham pair-fed, hyperammonemic, bile duct ligation

Brain ion and amino acid contents during edema development in hepatic encephalopathy.

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Brain edema in hepatic encephalopathy has been associated with circulating ammonia that is metabolized to glutamine. We measured alterations in blood chemistry and brain regional specific gravity and ion and amino acid contents in models of simple hyperammonemia and liver failure induced by daily

Astrocyte swelling in hepatic encephalopathy: molecular perspective of cytotoxic edema.

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Hepatic encephalopathy (HE) may occur in patients with liver failure. The most critical pathophysiologic mechanism of HE is cerebral edema following systemic hyperammonemia. The dysfunctional liver cannot eliminate circulatory ammonia, so its plasma and brain levels rise sharply. Astrocytes, the

Pathogenesis of hepatic encephalopathy and brain edema in acute liver failure.

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Neuropathologic investigations in acute liver failure (ALF) reveal significant alterations to neuroglia consisting of swelling of astrocytes leading to cytotoxic brain edema and intracranial hypertension as well as activation of microglia indicative of a central neuroinflammatory response. Increased

Hepatic encephalopathy: current management strategies and treatment, including management and monitoring of cerebral edema and intracranial hypertension in fulminant hepatic failure.

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OBJECTIVE Hepatic encephalopathy is a syndrome whose pathophysiology is poorly understood, for which we lack high-quality diagnostic tests and markers, and whose treatment has improved only slightly over the last several decades. Serum ammonia levels remain the diagnostic gold

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

Liver-brain proinflammatory signalling in acute liver failure: role in the pathogenesis of hepatic encephalopathy and brain edema.

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A robust neuroinflammatory response characterized by microglial activation and increased brain production of pro-inflammatory cytokines is common in acute liver failure (ALF). Mechanisms proposed to explain the neuroinflammatory response in ALF include direct effects of systemically-derived

HEPATIC COMA AND ANASARCA.

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Additional uses of the artificial kidney: selected cases of chronic renal failures; intractable edema; hepatic coma.

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[Brain edema. A cause of death in endogenous hepatic coma].

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