Urease poisoning in the dog

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Abstract
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.

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