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Results for “hyperammonemia”

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PubMed2006

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

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 (BDL), BDL pair fed, and BDL+HD. The BDL+HD rats were made hyperammonemic via an ammonia-containing diet that began 2 weeks after operation. One week later, the animals were sacrificed. BDL+HD rats displayed an increased level of cerebral ammonia and neuroanatomical characteristics of hepatic encephalopathy (HE), including the presence of type II Alzheimer astrocytes. Both BDL and BDL+HD rats showed activation of the inflammatory system. BDL+HD rats showed an increased amount of brain glutamine, a decreased amount of brain myo-inositol, and a significant increase in the level of brain water. In coordination tests, BDL+HD rats showed severe impairment of motor activity and performance as opposed to BDL rats, whose results seemed only mildly affected. In conclusion, the BDL+HD rats displayed similar neuroanatomical and neurochemical characteristics to human HE in liver cirrhosis. Brain edema and inflammatory activation can be detected under these circumstances.

Analysis of Variance↗
PubMed2006

Environmental heat stress, hyperammonemia and nucleotide metabolism during intermittent exercise.

This study investigated the influence of environmental heat stress on ammonia (NH3) accumulation in relation to nucleotide metabolism and fatigue during intermittent exercise. Eight males performed 40 min of intermittent exercise (15 s at 306+/-22 W alternating with 15 s of unloaded cycling) followed by five 15 s all-out sprints. Control trials were conducted in a 20 degrees C environment while heat stress trials were performed at an ambient temperature of 40 degrees C. Muscle biopsies and venous blood samples were obtained at rest, after 40 min of exercise and following the maximal sprints. Following exercise with heat stress, the core and muscle temperatures peaked at 39.5+/-0.2 and 40.2+/-0.2 degrees C to be approximately 1 degrees C higher (P<0.05) than the corresponding control values. Mean power output during the five maximal sprints was reduced from 618+/-12 W in control to 558+/-14 W during the heat stress trial (P<0.05). During the hot trial, plasma NH3 increased from 31+/-2 microM at rest to 93+/-6 at 40 min and 151+/-15 microM after the maximal sprints to be 34% higher than control (P<0.05). In contrast, plasma K+ and muscle H+ accumulation were lower (P<0.05) following the maximal sprints with heat stress compared to control, while muscle glycogen, CP, ATP and IMP levels were similar across trials. In conclusion, altered levels of "classical peripheral fatiguing agents" does apparently not explain the reduced capacity for performing repeated sprints following intermittent exercise in the heat, whereas the augmented systemic NH3 response may be a factor influencing fatigue during exercise with superimposed heat stress.

Adult↗
PubMed2004

Acute hemodialysis for hyperammonemia in small neonates.

Neonatal metabolic emergencies require a multidisciplinary team approach for supportive management that has increasingly come to feature renal replacement therapies in addition to nutritional support, the use of pharmaceutical agents, and testing to guide management and provide a definitive diagnosis. An increased appreciation for the mechanisms involved in ammonia neurotoxicity has placed greater emphasis on the need for its rapid yet safe resolution to optimize long-term prognosis. We examined our experience of intermittent hemodialysis (HD) and considered (1) the feasibility of HD in low-weight neonates, (2) the rate of decrease in ammonia, (3) complications during HD in small neonates weighing <4 kg presenting at University Children's Hospital between 1999 and 2002. Additionally, we review the current cellular and molecular mechanism of ammonia-induced brain injury. All patients tolerated intermittent HD and all required pressor agents. We primed all our patients with 20 U/kg of heparin and there was no subsequent need for further heparinization. We also noted that hemodynamic instability persisted during the first 1-2 h of the procedure and improved thereafter, as indicated by a decreased need for pressor agents. All neonates are alive to date. In conclusion, HD remains an effective and practical mode of renal replacement therapy having readily managed complications in preterm neonates weighing <4 kg with metabolic disorders.

Ammonia↗
PubMed2001

Extracorporeal dialysis in neonatal hyperammonemia: modalities and prognostic indicators.

We investigated the prognostic indicators in ten hyperammonemic neonates: four treated by continuous arteriovenous hemodialysis (CAVHD), four with continuous venovenous hemodialysis (CVVHD), and two with hemodialysis (HD). Plasma ammonium levels decreased significantly within the first 24 h irrespective of dialysis modality (from 1419 to 114 micromol/l, median values; P<0.0001). CVVHD achieved the highest ammonium clearance. HD provided highest ammonium extraction but clearance was hampered by severe hemodynamic instability. Five patients had a good outcome (normal at follow-up of 9-59 months), five had poor outcome (four died and one has severe neurological damage). Total coma duration was shorter in patients who had a good outcome (47+/-11 vs 78+/-13 h; P=0.02). Remarkably, only coma duration before dialysis determined this difference (22.2+/-10.1 vs 48.8+/-11.2 h; P=0.02). In cases with good outcome, coma duration was <33 h, whereas the others exceeded this limit. The prognosis was not related to dialysis modality, rapidity in reducing ammonium levels or to the underlying metabolic defect. In conclusion, results showed CVVHD to be the optimal modality for extracorporeal ammonium detoxification. However, the most relevant indicator for prognosis was coma duration before the start of dialysis. Therefore, major efforts should be made to refer patients quickly to highly specialized centers.

Coma↗
PubMed2005

Protein tyrosine nitration in hyperammonemia and hepatic encephalopathy.

Hepatic encephalopathy is seen as a clinical manifestation of a chronic low grade cerebral edema, which is thought to trigger disturbances of astrocyte function, glioneuronal communication, and finally HE symptoms. In cultured astrocytes, hypoosmotic swelling triggers a rapid oxidative stress response, which involves the action of NADPH oxidase isoenzymes, followed by tyrosine nitration of distinct astrocytic proteins. Oxidative stress and protein tyrosine nitration (PTN) are also observed in response to ammonia, inflammatory cytokines, such as TNF-alpha or interferons, and benzodiazepines with affinity to the peripheral benzodiazepine receptor (PBR). NMDA receptor activation was identified as upstream event in protein tyrosine nitration (PTN). Cerebral PTN is also found in vivo after administration of ammonia, benzodiazepines or lipopolysaccharide and in portocaval shunted rats. PTN predominantly affects astrocytes surrounding cerebral vessels with potential impact on blood-brain-barrier permeability. Among the tyrosine-nitrated proteins, glutamine synthetase, GAPDH, extracellular signal-regulated kinase and the PBR were identified. PTN of glutamine synthetase is associated with inactivation of the enzyme. Thus, factors known to trigger hepatic encephalopathy induce oxidative/nitrosative stress on astrocytes with protein modifications through PTN. The pathobiochemical relevance of astrocytic PTN for the development of HE symptoms remains to be established.

Animals↗
PubMed2002

[Fulminant coma: think hyperammonemia and urea cycle disorders].

The authors report the case of 14-year-old boy admitted for acute coma without neurological focal symptom. The only relevant finding was the death of one uncle after a coma in the year 1992. This coma was associated with an ammonia blood level of 344 mumol l-1 and it rapidly lead to cerebral death despite a symptomatic treatment. The diagnosis of hereditary ornithine transcarbamylase deficiency was confirmed by liver biopsy in the immediate post-mortem period. The authors recommend the measurement of blood ammonia in every coma without diagnosis, whatever patient's age.

Adolescent↗
PubMed2001

Cerebral energy metabolism in hepatic encephalopathy and hyperammonemia.

Hepatic encephalopathy (HE) is an important cause of morbidity and mortality in patients with severe liver disease. Although the molecular basis for the neurological disorder in HE remains elusive, elevated ammonia and its chief metabolite glutamine are believed to be important factors responsible for altered cerebral functions, including multiple neurotransmitter system(s) failure, altered bioenergetics, and more recently oxidative stress. Accumulated evidence suggests that direct interference of ammonia at several points in cerebral energy metabolism, including glycolysis, TCA cycle, and the electron transport chain, could lead to energy depletion. Additionally, recent studies from our laboratory have invoked the possibility that ammonia and glutamine may induce the mitochondrial permeability transition in astrocytes, a process capable of causing mitochondrial dysfunction. Altered mitochondrial metabolism appears to be an important mechanism responsible for the cerebral abnormalities associated with HE and other hyperammonemic states.

Brain↗