Pathogenesis of urea poisoning
Szegedi, B.; Juhász, B.
Acta Veterinaria Academiae Scientiarum Hungaricae 21(2): 291-306
1971
ISSN/ISBN: 0001-7205 PMID: 5160673 Document Number: 31369
In 28-45 kg ewes of the Comb Wool Merino breed fitted with a ruminal fistula, toxic doses of urea were administered intraruminally in various circumstances to determine their influence on NH3, urea and lactic acid contents, as well as pH of ruminal liquor, saliva, blood and urine. No toxic symptoms were noted when 1 g urea per kg body wt was infused over 20 min. during the third hour of a slow six-hour infusion of 60 g lactic acid in 20% soln., nor when 1.2 g/kg urea was administered four hours after 1 kg carbohydrate-rich whole meal had been given by fistula. Although the NH3 conc. in ruminal liquor rose considerably, ruminal pH stayed acid. The NH3 content of the blood was raised but did not reach the toxic level of 0.4-0.5 mMol/1. Urea conc. of blood and saliva likewise increased, but salivary secretion was reduced, so that less urea was carried by the saliva into the rumen. This reduction of salivary secretion was correlated with increased diuresis and a higher NH3 and urea conc. of the urine. It is concluded that the most important factor in preventing acute urea toxicosis is the activity of carbohydrate-fermenting processes in the urine, as this keeps the pH low and hence slows down urea hydrolysis and resorption of NH3. During infusion of ammonium acetate, it was found that the NH3 conc. of cerebrospinal fluid rose to only 20-30% of the blood level; however, the blood NH3 dropped sooner, which suggests that symptoms of NH3 toxicosis are not always related to the blood level.