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Certain compounds containing or liberating ammonium may induce the syndrome of impending hepatic coma in susceptible patients with hepatic cirrhosis or Eck fistula (1-4). This syndrome is often but not always associated with increased ammonium concentrations in the blood (5, 6). Although the origin and sources of elevated blood ammonium concentrations are not entirely clear, several factors contributing to them have been investigated. Decreased ammonium removal by the liver, resulting from either inadequate urea synthesis or from portal-systemic shunting of blood (7-10), is an important factor since increased arterial blood ammonium concentrations rarely occur if the liver and its circulation are normal. Elevated blood ammonium concentrations from an increased ammonium load are also observed in patients with liver disease. An increased load may result from the oral or intravenous administration of ammonium salts, amino acids and urea (1, 2, 11-13), from protein given orally (3, 14), and from gastrointestinal bleeding (15). Previous investigations of patients with hepatic decompensation have demonstrated that the extremities and brain, which contain systems active in ammonium metabolism, are important sites for the removal of ammonium from the circulating blood (16-18). The roles of these peripheral sites in ammonium metabolism were evaluated in the present study also. In some instances, the extremities and brain of patients with severe hepatic

AMMONIUM UPTAKE BY THE EXTREMITIES AND BRAIN IN HEPATIC COMA, 12