Urease poisoning in the dog

¹ Naval Medical Research Institute, National Naval Medical Center, Bethesda, Maryland

Ammonium intoxication in dogs was induced by intravenous administration of urease. This method affords a unique preparation for the study of ammonia metabolism in vivo, since, within limits, a self-perpetuating, cyclic release of ammonia is achieved. Through the action of the enzyme, NH₃—N is released from urea to be resynthesized via the ornithine-arginine cycle, operating in liver, to urea, from which in turn the ammonia nitrogen is released. Measurements of blood NH₃—N, plasma NH₃—N, BUN and plasma glutamine before and at 5, 30, and 60 minutes post intoxication show a highly significant increase in plasma glutamine and NH₃—N levels and a decrease in BUN following ammonium intoxication. In showing that glutamine synthesis plays a major role in the clearance of an "overload" of NH₃—N from the blood, and presumably other tissues, these results are in good agreement with the findings of other investigators.

Note:
With the Assistance of Paul J. Stonestreet and Paul W. Johnson