Hepatic Coma and Ammonia Metabolism in Dogs

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Abstract
HEPATIC COMA or encephalopathy may be classified as "spontaneous" with liver failure but little rise in blood ammonia, or "exogenous" with toxic symptoms from very high ammonia levels.1 The latter occurs after portal-systemic vein shunting operations and is generally attributed to the inability of the liver to detoxify ammonia through the normal pathways of the Krebs-Hensleit urea cycle. It is thought that in "spontaneous" hepatic encephalopathy, on the other hand, many enzymatic and metabolic systems simultaneously are adversely affected in the liver leading to coma refractory to treatment. This variety is therefore not characterized by the predominating influence of one biochemical defect. Clinically the gradation is not sharp and many intermediate states are observed. Both types of coma were observed in the laboratory in dogs following portacaval shunt operations in which "Eck's fistulae" were formed. In a previous report it was pointed out that the high blood ammonia

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