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HAROLD A. HARPER, Ph.D.; JOHN Q. OWSLEY, Jr., M.D.

AMA Arch Surg. 1958;76(5):766-768.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The intravenous administration of ammonium chloride is sometimes used in the treatment of patients with severe alkalosis. It has been suggested that the toxic reactions occasionally encountered when ammonium chloride is administered may be due to ammonia intoxication.^1-3 It is possible, therefore, that the toxicity of ammonium chloride solutions may be prevented if the increase in the blood ammonia that follows their administration can be controlled.

In various clinical states in which ammonia intoxication is a pathogenic factor, glutamic acid has been used to lower the blood ammonia.^4,5 This amino acid may lower the blood ammonia by forming glutamine, a reaction in which one mol of ammonia is utilized per mol of glutamine formed. Urea formation is quantitatively a more important metabolic route for disposal of ammonia than is glutamine formation. Urea production and a consequent lowering of the blood ammonia can be enhanced by the intravenous administration . . . [Full Text PDF of this Article]

Author Affiliations
San Francisco

From the Surgical Research Laboratories of the University of California School of Medicine.

Footnotes
Read at the 65th Annual Meeting of the Western Surgical Association, Salt Lake City, Nov. 22, 1957.

Supported by a grant from the National Institute for Arthritis and Metabolic Diseases (A-1053) and the Christine Breon Fund for Medical Research.

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