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At least 73 records · Page 4Linked to original sources
PubMed1984

Effect of charcoal hemoperfusion on amino acid disturbance in experimental hepatic coma.

Using the galactosamine induced hepatic coma rat model, we studied the effects of coated charcoal hemoperfusion on amino acids in plasma and CSF in grade III hepatic coma. We found that 1 hour of hemoperfusion significantly reduced AAAs and BCAAs in plasma and increased the molar ratio of BCAA:AAA. When rats in grade III coma were treated with 2 consecutive 1-hour hemoperfusions, the substantial reduction of plasma AAAs resulted in a significant decrease of AAA levels in CSF.

Adsorption↗
PubMed1979

A longitudinal study of tryptophan involvement in hepatic coma.

Previous cross-sectional studies have demonstrated that hepatic coma is associated with abnormally high levels of plasma free tryptophan. Establishment of a more definitive relationship between this biochemical abnormality and hepatic coma requires an evaluation of biochemical changes in individual patients as they undergo alterations in the function of their central nervous systems. The present report is an evaluation of tryptophan and substances believed to influence its entry into the brain in six patients whose clinical status progressed from hepatic coma to complete recovery. Consistent significant decreases in plasma free tryptophan and free fatty acids were demonsrated to occur as the patients recovered. No consistent changes, however, were found in the plasma levels of the amino acids which have been reported to compete with tryptophan for transport across the blood-brain barrier, except for leucine which was significantly decreased in all six patients upon recovery from coma. Assay of lumbar cerebrospinal fluid for both tryptophan and the serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), showed no consistent changes as the patients recovered from hepatic coma.

Adult↗
PubMed1986

Lack of evidence for impaired dopamine receptor function in experimental hepatic coma in the rabbit.

In order to determine whether hepatic coma is associated with an altered sensitivity of the dopamine (DA) receptor in the brain, the activity of DA-sensitive adenylate cyclase was assayed in homogenates from the corpus striatum of normal rabbits and rabbits with galactosamine-induced fulminant hepatic failure by measuring cyclic adenosine monophosphate production from adenosine triphosphosphate radioimmunochemically. The kinetic properties of adenylate cyclase in control rabbits and rabbits with hepatic coma were similar (Km, 17 +/- 2.9 (S.E.M.) vs 20 +/- 6.4 mM; Vmax, 816 +/- 58 vs 1054 +/- 233 pmol/mg protein/5 min, respectively). Hepatic coma was not associated with any changes in the responses of the DA receptor-adenylate cyclase system to DA (maximum stimulation 60% vs 57%), sodium fluoride (maximum stimulation 104% vs 132%), or a D-2 DA receptor agonist (maximum inhibition 18% vs 12%). These findings make it unlikely that alterations of dopaminergic neurotransmission play an important role in the pathogenesis of hepatic coma.

Adenylyl Cyclases↗
PubMed1988

Regional brain GABA metabolism and release during hepatic coma produced in rats chronically treated with carbon tetrachloride.

Hepatic coma was induced in rats chronically treated with CCl4, by means of a single injection of ammonium acetate. The activities of glutamate decarboxylase (GAD) and GABA transaminase (GABA-T), as well as the synaptosomal uptake and release of [3H]GABA, were measured in the following brain areas of the comatose rats: cortex, striatum, hypothalamus, hippocampus, midbrain and cerebellum. Hepatic coma was associated with a general decrease of GAD activity, whereas GABA-T activity was diminished only in the hypothalamus, striatum and midbrain. During hepatic coma, the K+-stimulated [3H]GABA release was notably diminished in the striatum and cerebellum, whereas a significant increase was observed in the hippocampus. [3H]GABA uptake increased in most regions after CCl4 treatment, independently of the presence of coma. The results indicate that GABAergic transmission seems to be decreased in most cerebral regions during hepatic coma.

4-Aminobutyrate Transaminase↗