Abstract
SUMMARYThe intravenous (i.v.) infusion of solutions of ammonium salts into sheep produced a toxic condition in which the clinical signs, pathological findings and concentrations of ammonia in the venous blood were comparable with those found in urea poisoning, provided that the urea and ammonia toxicoses were induced over similar time intervals. Our results indicate that urea toxicosis in ruminants is due to the toxic effects of ammonia. Although the clinical signs resulting from the i.v. infusion of ammonium chloride, acetate and hydroxide showed some relationship to the basicity of the compounds, alkalosis did not appear to be a necessary prerequisite for ammonia toxicosis.The tolerances of sheep to orally administered urea and i.v. infused ammonium salt solutionswere shown to be positively related to dietary nitrogen intake. These results and the observations reported by Payne & Morris (1969) that the concentrations of urea-cycle enzymes per unit of liver tissue were markedly affected by dietary nitrogen intake suggest that supplementation of ruminants grazing low-protein pastures with urea, occurs at a time when their tolerances to an over-dose of urea are minimal.The i.v. administration of arginine and of y-amino butyric acid plus glucose did not appear to be of practical value in preventing urea poisoning.
Publisher
Cambridge University Press (CUP)
Subject
Genetics,Agronomy and Crop Science,Animal Science and Zoology
Cited by
20 articles.
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