Abstract
It is proposed that hyperammonæmia in liver cirrhosis or after portacaval shunt contributes to plasma neutral aminoacid imbalance and to increased activity of the blood-brain neutral aminoacid transport system. Plasma neutral aminoacid concentrations are deranged, partly, but not completely, because ammonia stimulates glucagon secretion; a high rate of gluconeogenesis and hyperinsulinæmia follow. Brain uptake of neutral aminoacids rises because ammonia stimulates brain-glutamine synthesis, which results in rapid exchange of brain glutamine for plasma neutral aminoacids. Hyperammonæmia therefore contributes to encephalopathy indirectly, by raising the brain concentration of neutral aminoacids which alter neurotransmitter metabolism, rather than directly, by toxic effects on neuronal metabolism.
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