hepatic encephalopathy/kaalium

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Acute hepatic encephalopathy decreases potassium-evoked calcium uptake in astrocytes but not in synaptosomes of the rat.

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45CaCl2 uptake at low (5 mM), and high, depolarizing (65 mM) KCl concentration was measured in a fraction enriched in astrocytes, a crude mitochondrial-synaptosomal (P2) preparation and in purified synaptosomes derived from normal rats and from rats with thioacetamide-induced acute hepatic

Potassium-evoked neuronal release of serotonin in experimental chronic portal-systemic encephalopathy.

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Portal-systemic encephalopathy (PSE) is associated with an increased brain tissue turnover of serotonin (5-HT). Despite increased 5-HT metabolism, brain 5-HT release in rats with a portacaval shunt (PCS) seems to be unaltered. Although this may indicate that the overall 5-HT output is unaltered in

Release of [3H]dopamine from striatal and cerebral cortical slices from rats with thioacetamide-induced hepatic encephalopathy: different responses to stimulation by potassium ions and agonists of ionotropic glutamate receptors.

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The effects of depolarizing stimuli; high (50 mM) potassium ions and the glutamate receptor agonists N-methyl-D-aspartate, kainate and 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) on the release of newly-loaded [3H]dopamine were studied in frontal cortical and striatal slices from control

Treatment with a potassium-iron-phosphate-citrate complex improves PSE scores and quality of life in patients with minimal hepatic encephalopathy: a multicenter, randomized, placebo-controlled, double-blind clinical trial.

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OBJECTIVE Minimal hepatic encephalopathy (MHE) is one of the possible complications of liver cirrhosis. In this study, a potassium-iron-phosphate-citrate complex was analyzed for its efficacy and safety in the treatment of MHE, as this complex is supposed to bind to the major pathogenic factor of

Relation of potassium depletion to renal ammonium metabolism and hepatic coma.

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Further comments on the importance of serum potassium concentrations on early hepatic encephalopathy.

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BODY AND SERUM POTASSIUM IN LIVER DISEASE. II. RELATIONSHIPS TO ARTERIAL AMMONIA, BLOOD PH, AND HEPATIC COMA.

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Effects of high-normal and low-normal serum potassium levels on hepatic encephalopathy: facts, half-facts or artifacts?

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[Disorders of kidney function in hepatic coma].

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Renal function was evaluated in 80 patients with hepatic coma stage III-IV (24 patients had acute fulminant hepatic failure, 48 patients chronic hepatic failure, 8 patients had a mixed form). Urea, creatinine and electrolytes were measured in plasma and urine as well as creatinine clearance and

Prognostic significance of hypokalemia in hepatic encephalopathy.

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OBJECTIVE The aim of this study was to investigate whether hypokalemia prognosticates outcomes in hepatic encephalopathy. We also examined other potential prognostic variables such as serum pH, systemic vascular resistance (SVR) and serum ammonia levels. METHODS Patients with cirrhosis who were

[Ammoniemia in portosystemic encephalopathy--diagnostic, differential diagnostic and prognostic significance].

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One year prospective study of 25 cirrhotic patients with portal systemic encephalopathy (PSE) admitted to the Emergency Care Centre in Belgrade was performed in order to investigate the significance of clinical, biochemical and electroencephalographic (EEG) parameters and blood ammonia in the

Taurine release from brain slices in thioacetamide-induced hepatic encephalopathy in rats.

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The possible involvement of taurine in the pathogenesis of hepatic encephalopathy was studied in rats injected with thioacetamide. Spontaneous release of exogenous labeled taurine was not affected in any brain area studied, but the potassium-stimulated release was enhanced in the striatum in

[Portal vein thrombosis associated with hepatic encephalopathy].

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A 54-year-old man who had been administered chlormadinone acetate 3 months after prostatectomy for prostate cancer, acutely developed disorientation and memory disturbance. Six days later, he experienced high grade fever and epigastralgia. He was suspected to have hepatic encephalopathy, because the

Predictive factor for hepatic encephalopathy in cirrhotic patients who presented with acute variceal bleeding.

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BACKGROUND Cirrhotic patients who were hospitalized due to acute variceal bleeding and subsequently developed hepatic encephalopathy during hospital stay had dreadful outcome and high mortality rate. Recommendations regarding management and prevention of encephalopathy in these patients are not

Incisional hernia as an unusual cause of hepatic encephalopathy in a 62-year-old man with cirrhosis: a case report.

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BACKGROUND Hepatic encephalopathy may be initiated by many factors such as gastrointestinal bleeding, infections, fluid and electrolyte disturbances. Hypokalemia is one of the most commonly encountered electrolyte abnormalities causing hepatic encephalopathy in patients with cirrhosis. METHODS We

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