THE CEREBRAL AND PERIPHERAL UPTAKE OF AMMONIA IN LIVER DISEASE WITH AN HYPOTHESIS FOR THE MECHANISM OF HEPATIC COMA 12

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Abstract
Femoral arterial and jugular bulb ammonia levels in 38 patients were determined by microdiffusion. All 21 patients without liver disease had arterial levels of less than 1.0 ug ammonia [image]/ml. The maximum cerebral uptake of ammonia was 0.12 [mu]g/ ml and the mean -0.05 Mg, or a slight evolution of ammonia. All 17 patients with liver disease had arterial levels greater than 1.0 [mu]g/ml (range 1.39-8.44 [mu]g/ml). The uptake of ammonia by the brain was between 0.12 and 2.40 [mu]g/ml and was proportional to the arterial level. Muscle uptake of ammonia was also shown in 7 cases, and in 3 cases in which both cerebral and peripheral uptake were measured, they were approximately equal. Since muscle takes up ammonia, a false impression of the actual blood ammonia level arriving at the brain results if venous blood alone is measured. Hepatic coma maybe based on the reversal of glutamic dehydrogenase. The synthesis of glutamic acid by brain in response to high arterial ammonia levels results in a depletion of alphaketoglutarate in brain, and eventual stoppage of the Krebs cycle.