Role of hyperammoniemia in lethal outcome of acute intoxication by cyclophosphamide in rats
The administration of cyclophosphamide in doses of LD50. 0.73-3.64 to rats was followed by hyperammoniemia stipulated by an intensified outflow of ammonia from the gastrointestinal tract into the portal of caudal caval vain by-passing the liver, and by a lagged behind synthesis of glutamine and urea in the liver in relation to the income of ammonia into the portal vein. An enhanced ammonia pool in the lumen of the digestive tract aggravated the intoxication by cyclophosphamide and added symptoms of acute intoxication by ammonia salts.. Thus, hyperammoniemia is one of thanatogenesis mechanisms at acute intoxication by cyclophosphamide.