Thesis - Open Access
Master of Science (MS)
Urea was introduced as an economical nonprotein nitrogen source for ruminant animals. In the gastrointestinal tract, urea is hydrolyzed in the presence of bacterial urease to ammonia and carbon dioxide. The liberated ammonia is utilized by rumen microorganisms for amino acid synthesis. Ammonia not used by microorganisms diffuses through the gastrointestinal lining and is transported to the liver by blood, where enzymes synthesize urea by combining two moles of ammonia and one mole of carbon dioxide. The nontoxic urea is excreted by the kidney or secreted with saliva and other digestive fluids for recycling. Ammonia intoxication occurs when more ammonia is produced and absorbed than can be detoxified by the liver. Ammonia, predominately in the form of ammonium ion, produces toxicity symptoms which include hyperpnea, ataxia, muscle tremors, convulsions, tetany, and death. Numerous investigations have been conducted concerning the metabolic alterations and clinical signs in acute ammonia intoxication, however there is inadequate information concerning stability of ammonia in postmortem tissues. The purpose of this study was to investigate the postmortem stability of ammonia in sheep tongue, liver, and kidney tissues following acute ammonia intoxication. Liver and kidney tissues were collected because of their metabolic significance. Tongue tissues were collected because of easy access, which could provide a simple method of obtaining diagnostic tissues without opening the carcass.
Library of Congress Subject Headings
Ammonia in animal nutrition
Number of Pages
South Dakota State University
Jaquette, Dale L., "Tissue Ammonium Nitrogen in Sheep Tongue, Liver and Kidney Following Death by Ammonia Intoxication" (1972). Electronic Theses and Dissertations. 4789.