hyperammonemia/hypoxia

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Hypoxia, hyperammonemia, and cerebrospinal fluid metabolites.

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During hemorrhagic shock, increased uptake of NH3 from the gut with inadequate compensation by the liver results in hyperammonemia. The effect on brain metabolism of acute hyperammonemia alone, as compared with normocapnic hypoxia, was investigated in 11 pentobarbital anesthetized (30 mg/kg) dogs.

[Correlations among hypoxia, hypercapnia and hyperammonemia in patients with cor pulmonale decompensatum].

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The correlation between ammonia concentration of the plasma and blood pH, blood gas values was examined in 28 patients with chronic cor pulmonale decompensatum. In cases with central nervous symptoms were found a significant negative correlation between ammonia concentration of the plasma and

Hyperammonemia in the neonate with hypoxia.

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Preservation of cerebral blood flow responses to hypoxia and arterial pressure alterations in hyperammonemic rats.

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Acute hyperammonemia causes cerebral edema, elevated intracranial pressure and loss of cerebral blood flow (CBF) responsivity to CO2. Inhibition of glutamine synthetase prevents these abnormalities. If the loss of CO2 responsivity is secondary to the mechanical effects of edema, one would anticipate

Cerebral blood flow in hyperammonemia: heterogeneity and starling forces in capillaries.

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In the brain hyperammonemia interferes with ion homeostasis, membrane potentials, neurotransmission, and neurotransmitter recycling and reduces metabolic rates for oxygen and glucose. Because, cerebral blood flow (CBF) is closely coupled to metabolism, CBF is most often reduced in diseases

Impaired pial arteriolar reactivity to hypercapnia during hyperammonemia depends on glutamine synthesis.

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OBJECTIVE Acute hyperammonemia causes glutamine and water accumulation in astrocytes and loss of the cerebral blood flow response selectively to CO2. We tested whether extraparenchymal pial arterioles not subjected directly to mechanical compression by swollen astrocyte processes also lose

Preserved hypocapnic pial arteriolar constriction during hyperammonemia by glutamine synthetase inhibition.

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Ammonia intoxication, which results in astrocytic edema and glutamine accumulation, blocks cerebral vasodilation during hypercapnia but not during hypoxia. Ammonia's effect on blood flow during hypocapnia is unclear, with some brain regions showing a paradoxical increase in flow. Here, we studied

The utility of EEG monitoring in neonates with hyperammonemia due to inborn errors of metabolism.

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BACKGROUND Continuous EEG studies demonstrate that neonates with seizures due to cerebral pathology, such as hypoxia ischemia, exhibit predominantly electrographic seizures (i.e. those only detected with EEG because they lack clinical features). Previous small case series demonstrate EEG changes and

Reversible brain swelling in crucian carp (Carassius carassius) and goldfish (Carassius auratus) in response to high external ammonia and anoxia.

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Increased internal ammonia (hyperammonemia) and ischemic/anoxic insults are known to result in a cascade of deleterious events that can culminate in potentially fatal brain swelling in mammals. It is less clear, however, if the brains of fishes respond to ammonia in a similar manner. The present

Prognostic values of blood ammonia and partial pressure of ammonia on hospital arrival in out-of-hospital cardiac arrests.

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OBJECTIVE Outcome prediction for out-of-hospital cardiac arrest (OHCA) is of medical, ethical, and socioeconomic importance. We hypothesized that blood ammonia may reflect tissue hypoxia in OHCA patients and conducted this study to evaluate the prognostic value of ammonia for the return of

Nonketotic hyperglycinemia in two siblings with neonatal seizures.

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Seizures are a common problem in neonates. Differential diagnoses include infection, trauma, hypoxia and congenital metabolic disorders. Among these, congenital metabolic disorder is less familiar to general pediatricians. We report two patients with nonketotic hyperglycinemia (NKH), a rare and

[Present-day therapy of hepatic encephalopathy (author's transl)].

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The ammonia hypothesis is the most likely explanation for the pathogenesis of hepatic encephalopathy in cirrhosis patients. Reduction of hyperammonemia is therefore the most consistent therapy. From this point of view, the antibiotics have a central significance for the reduction of ammonia

Ostroe tyazheloe peroral'noe otravlenie 1,4-butandiolom i etanolom s razvitiem komatoznogo sostoyaniya.

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A case of acute oral poisoning by 1.4-butanediol, complicated by the development of severe hypoxia in a 34-year-old patient actively engaged in bodybuilding, is presented. The psychoactive substance was used by the patient to increase sexual activity and physical stamina. The duration of systematic

Relationship between oxidative stress and brain swelling in goldfish (Carassius auratus) exposed to high environmental ammonia.

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Buildups of ammonia can cause potentially fatal brain swelling in mammals, but such swelling is reversible in the anoxia- and ammonia-tolerant goldfish (Carassius auratus). We investigated brain swelling and its possible relationship to oxidative stress in the brain and liver of goldfish acutely

Neonatal congenital lactic acidosis with pyruvate carboxylase deficiency in two siblings.

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The authors report 2 familial cases of neonatal congenital lactic acidosis with pyruvate carboxylase deficiency in the liver. In both cases, disorders started immediately after birth and were characterized by major neurological symptoms, acute metabolic acidosis with hyperketonemia and

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