Is increased ammonia liberation after bleeding in the digestive tract the consequence of complete absence of isoleucine in hemoglobin? A study in pigs

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Abstract
A variable protein-induced toxicity has been reported in liver disease. The aim of this study was to establish the cause of increased ammonia liberation in the gut after intraluminal bleeding. Therefore, blood was sampled from catheterized piglets [20 ± 0.8 kg (means ± S.E.); n = 10] to determine ammonia, urea and amino acid levels before and 1, 2, 3 and 6 hr after a standard pig meal (750 gm, 12% protein). After 1 week, this procedure was repeated after ingestion of an isonitro-genous amount of bovine whole blood (400 ml). In a second series of experiments, the same procedures were performed after ingestion of plasma, whole blood, eryth-rocytes and feed. Electromagnetically measured total intestinal, small and large bowel flow was not significantly influenced by the type of meal ingested. Portal ammonia release was significantly increased 2-fold after a blood meal, whereas intestinal glutamine utilization did not increase. Plasma urea levels were increased 200 to 300% after whole blood and erythro-cytes, whereas after ingestion of plasma, urea levels were similar to values in controls. Glutamine utilization was not different among the various groups and occurred predominantly in the small bowel. In the fasted state, small bowel glutamine utilization paralleled ammonia production. In the fed state, this equimolar relationship could not be assessed because luminal glutamine utilization could not be determined. Isoleucine levels decreased to 25% of fasting levels. Analysis of blood constituents revealed a complete lack of isoleucine in the hemoglobin molecule. Net total α-amino-nitrogen absorption was doubled after a blood meal. The highest absorption was found in the small bowel. These findings lead us to hypothesize that, due to complete lack of isoleucine in hemoglobin, ingestion of blood into the gut presents the organism with protein of low biological value, leading to decreased protein synthesis and to net protein degradation, which in turn may result in increased ammonia- and ureagenesis.