Plasma Amino Acid Imbalance and Hepatic Coma
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Cirrhosis of the liver is a major disease with severe consequences to the patient, including coma. The causation of hepatic coma nevertheless continues to be the subject of speculation. For some years, it was postulated that ammonia formed in the intestine by bacterial action passed into the general circulation as a result of the liver failure and was responsible for the onset of coma. This explanation is, however, in conflict with data such as the studies of COHN and CASTELL (2), in which the electroencephalogram of patients with cirrhosis failed to respond to induction of acute hyperammonemia. It has been suggested by FISCHER and BALDE S SARIN I (6) that amines formed in the gut may pass into the general circulation in hepatic cirrhosis and become transformed in the brain to derivatives that compete with endogenous neurotransmitters. Specifically, FISCHER and BALDESSARINI present evidence that tyramine, formed by the intestinal flora from tyrosine, is a precursor of octopamine in the brain and that this latter displaces the normal adrenergic transmitters dopamine and norepinephrine.
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