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Ammonia toxicity in the ruminant

Published online by Cambridge University Press:  27 March 2009

D. Lewis
D. Lewis
Affiliation:
A.R.C. Institute of Animal Physiology, Babraham, Cambridge, andUniversity of Nottingham, School of Agriculture, Sutton Bonington, Loughborough
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Extract

1. The normal level of blood ammonia in the sheep seems to be somewhat higher than in nonruminants.

2. The toxicity of ammonium acetate, ammonium chloride or urea placed in the rumen follows different metabolic pathways. In the case of the chloride there is an uncomplicated metabolic acidosis which is not, however, adequate to account for the toxic symptoms. When the acetate is administered there is also a respiratory alkalosis and in the presence of urea the changes in the acid-base status, though interesting, do not account for the toxicity.

3. The toxicity is almost certainly due finally to a direct effect of the circulating ammonium ion level though in the case of urea, there is an earlier effect that may be of a pharmacological type and is less severe.

4. The organisms within the rumen rapidly reach a maximum level of adaptation (7 days) to handle large quantities of ammonia by a synthetic pathway.

5. The intravenous administration of L-arginine did not markedly ameliorate the ammonia toxicity.

Type
Research Article
Information
The Journal of Agricultural Science , Volume 55 , Issue 1 , August 1960 , pp. 111 - 117
Copyright
Copyright © Cambridge University Press 1960

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References

REFERENCES

Annison, E. F., Lewis, D. & Lindsay, D. B. (1959a) J. Agric. Sci. 53, 34.CrossRefGoogle Scholar
Annison, B. F., Lewis, D. & Lindsay, D. B. (1959 b). J. Agric. Sci. 53, 42.CrossRefGoogle Scholar
Bessman, S. P. (1958). Biochemistry of the Central Nervous System, p. 141. Proc. 4th Int. Cong. Biochemistry, Vienna. Pergamon Press.Google Scholar
Davenport, H. W. (1958). The ABC of Acid-Base Chemistry, 4th ed.Chicago Press.Google Scholar
Dinning, J. S., Briggs, H. M., Gallup, W. D., Orr, H. W. & Bulter, R. (1948). Amer. J. Physiol. 153, 41.CrossRefGoogle Scholar
Greenstein, J. P., Winitz, M., Gullino, P. & Birnbaum, S. M. (1955). Arch. Biochem. Biophys. 59, 320.CrossRefGoogle Scholar
Gullino, P., Winitz, M., Birnbaum, S. M., Cornfield, J., Otey, M. C. & Greenstein, J. P. (1955). Arch. Biochem-Biophys. 58, 253.CrossRefGoogle Scholar
Hale, W. H. & King, R. P. (1955). Proc. Soc. Exp. Biol. N.Y., 89, 112.CrossRefGoogle Scholar
Head, M. J. & Rook, J. A. F. (1955). Nature, Lond., 176, 262.CrossRefGoogle Scholar
Lewis, D. (1957). J. Agric. Sci. 48, 438.CrossRefGoogle Scholar
Lewis, D., Hill, K. J. & Annison, E. F. (1957). Biochem. J. 66, 587.CrossRefGoogle Scholar
Lewis, D. & McDonald, I. W. (1958). J. Agric. Sci. 51, 108.CrossRefGoogle Scholar
McDonald, I. W. (1948). Biochem. J. 42, 584.CrossRefGoogle Scholar
Reid, J. T. (1953). J. Dairy Sci. 36, 955.CrossRefGoogle Scholar
Repp, W. W., Hale, W. H., Cheng, E. W. & Burroughs, W. (1955). J. Anim. Sci. 14, 118.CrossRefGoogle Scholar
Roberts, K. E., Thompson, F. G., Popell, J. W. & Vanamee, P. (1956). J. Appl. Physiol. 9, 367.CrossRefGoogle Scholar
Rosenthal, T. B. (1948). J. Biol. Chem. 173, 25.CrossRefGoogle Scholar
Van Slyke, D. D. & Neill, J. M. (1924). J. Biol. Chem. 61, 523.CrossRefGoogle Scholar
Walshe, J. M. (1953) Lancet, 1, 1075.CrossRefGoogle Scholar
Wechsler, R. L., Crum, W. & Roth, J. L. A. (1954). Clin. Res. Proc. 2, 74.Google Scholar
Wood, F. J. Y. (1955). Clin. Sci. 14, 81.Google Scholar