Jan 1, 1975

Cerebral manifestations in the hepatic coma syndrome (author's transl)

Wiener klinische Wochenschrift. Supplementum
J Funovics

Abstract

The pathogenesis of hepatic encephalopathy has been investigated in a two-stage devascularization model in the rat with portavacal shunt and hepatic artery ligation. There is a significant increase in brain octopamine and phenylethanolamine and a decrease in brain norepinephrine (NE) 6 to 9 hours after hepatic artery ligation. The depletion of NE seems the sequel of diminished synthesis in the presence of an unaltered turnover rate, due to a blockade of tyrosine hydroxylase either by accumulation of false neurochemical transmitters or by phenylalanine. It is most marked in the cortex and midbrain. The high-energy phosphate compounds, ATP, phosphocreatine and glucose-6-phosphate are not diminished in hepatic coma, nor is glucose, indicating that other mechanism are involved in the pathogenesis of metabolic state by the increased ammonia level. "intestinal sterilization" and total colectomy have no significant effect on the ammonia level, but cause a decrease in the level or aromatic precursor amino acids in the plasma and brain, with normalization of the level of cerebral transmitters. These results permit the formulation of a unified concept of the hepatic coma syndrome and its clinical manifestations such as flapping tremor, t...Continue Reading

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Mentioned in this Paper

Metabolic Process, Cellular
Pathogenic Aspects
Octopamine
Taenia Coli
Cortex Bone Disorders
Adrenal Cortex Diseases
Pathogenesis
Aromatic Amino Acid Decarboxylase Deficiency
Phosphocreatine
Amino Acids, I.V. solution additive

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