Abstract
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.