Abstract
Summary
The arteriovenous difference of ammonia has been investigated in a variety of conditions and has been found to be elevated in hepatic coma, as has been the arterial level of blood ammonia. The evidence for a significant uptake of ammonia in comatose patients with liver disease suggests a mechanism for hepatic coma. This mechanism could be the reductive amination of ketoglutaric acid to form glutamate with the concomitant removal of significant amounts of ketoglutarate, preventing Krebs cycle regeneration.
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