Abstract
It is commonly believed that the digestion of intraluminal blood by colonic bacteria is the primary cause of increased ammonia production after upper gastrointestinal hemorrhage. To evaluate the role of the small intestine in ammonia production, blood, amino acids, or water (5 mL/kg) was administered as a meal or enema to awake dogs with chronic indwelling catheters. After blood meals, intestinal ammonia production increased rapidly to peak at 60 minutes and returned to basal levels. This response was mimicked by the gastric administration of ammoniagenic amino acids. No change in ammonia production occurred with water administration. In contrast, colonic blood administration resulted in a gradual rise in ammonia production, and peaked at 150 minutes. Amino acid enemas resulted in a similar but somewhat more rapid response. No change occurred with water enemas. After gut decontamination, ammonia production did not increase after blood enemas. However, the rapid increase in ammonia production persisted after blood meals. It is concluded that both the small bowel and colon participate in the augmented ammonia production that occurs after upper gastrointestinal hemorrhage. Gut decontamination reduces ammonia production by altering the colonic microflora, but is not specific therapy directed towards amino acid metabolism by the enterocytes of the small bowel and thus, does not alter the ammonia produced by the small intestine.