Abstract
Toxicity of ammonium salts and urea was examined in rabbits and goats by feeding.
1. If blood levels of NH3-N were below 0.9mg and those of urea-N below 30mg per 100cc, these values were regarded as normal in rats, rabbits and goats.
2. Rats idjected with ammonium carbonate or urea solutions into the heart died when N content of the injected solution in 100cc of blood reached 8mg in the former case or 1500mg in the later case.
3. Aqueous solutions of ammonium carbonate or chloride were administered into the stomach or rumen of rabbits and goats with a catheter. The rabbits died at 1-gram urea-equivalent level (calculated on N base) per kg of body weight and the goats died at 0.8-g urea-equivalent level. Toxication symptoms and progresses in the goats closely resembled those of urea toxicosis following the increase of NH3-N content in blood. There was no considerable difference between rabbits and goats with regard to a toxic dose of ammonium salts, and the increase of urea-N content in blood was little in both animals.
4. Period of time required for the occurrence of symptoms and the course of toxicosis were prolonged or reduced according to pH of the solution and quantity of stomach contents.
5. On administration of urea solution into the stomach with a catheter, rabbits died at 6-g per kg level. Symptoms and progresses closely resembled ammonium-salt toxicosis. But, rabbits administered urea previously seemed to stand the urea given succeedingly. No appreciable symptom was shown in rabbits when they were administered with 1g of per kg of urea in phosphate buffer or in the form of dumpling.
6. NH3-N and urea-N contents in the blood of the portal and hepatic veins and the heart were determined in normal, survived, and dead animals. NH3-N contents in the blood of these three vessels decreased in the order above mentioned in each animal, and those of the portal vein were about two times larger than those of the heart in administered animals. Therefore, it was assumed that urea was cleft bofore absorbed into the portal vein, hat its N was transformed to NH3-N, that the liver controled NH3-N so as not to flow into the circulating blood stream and that the urea passed through the liver apparently unchanged.
7. Blood NH3-N and urea-N contents increased with the progress of toxicosis and reached the maximum values at death. In this case, symptoms did not appear, despite of the urea-N increase, until NH3-N content reached some level.
8. Administration of urea caused an increase of NH3-N level in the contents of the alimentary canal in rabbits.
9. From these results it was deduced that an immediate cause of urea toxicity consisted in the increased portion of NH3-N content in the blood.
