Ammonia toxicity in cattle. V. Ammonia concentration of lymph and portal, carotid and jugular blood after the ingestion of urea.

Four rumen-fistulated Holstein steers were fitted with cannulas for the collection of portal, jugular and carotid blood. In addition, the thoracic duct of one steer was cannulated for the collection of lymph. Steers were given .125, .25 or .5 g urea/kg body weight 16 hr after a previous feeding. Within 5 min after the administration of the .5-g dose, rumen ammonia increased from 9.7 to 32.0 mg/100 ml, rumen pH from 6.47 to 7.87; portal blood ammonia from 1.02 to 8.01 mg/100 ml, carotid blood ammonia from .18 to 1.17 mg/100 ml and jugular blood ammonia from .13 to .36 mg/100 ml. Lymph ammonia increased from .22 to .32 mg/100 ml within 15 minutes. The .125- and .25-g doses or urea produced proportionate changes. In a second experiment, three Jersey cows were given .5 g urea/kg body weight, and the rates at which urea appeared in carotid and jugular blood were determined. Only small amounts of urea appeared in carotid and jugular blood during the first 5 min after dosing, but the concentrations then increased slowly but progressively. We concluded that because carotid blood ammonia concentration increased so rapidly after dosing with urea, ammonia must leak past the liver, and it is therefore unlikely, that there is a liver threshold for ammonia which must be exceeded before ammonia will reach the carotid artery. The marked difference in ammonia concentrations in carotid and jugular blood suggests that the brain takes up ammonia rapidly. While some ammonia is absorbed via the lymph, and thus bypasses the liver, the lymph does not appear to be a major contributor of ammonia to carotid blood.

Characterization of endotoxin from the rumen bacterium Megasphaera elsdenii.

Phenol-water extraction of Megasphaera elsdenii, a predominant gram-negative coccus in rumens of cattle fed high-grain diets, yielded material that exhibited typical characteristics of endotoxin. The extract was lethal to mice and to chicken embryos, caused biphasic fever in rabbits, leukopenia in mice, and local and generalized Shwartzman reactions; and induced tolerance to the lethal effect of the endotoxin in mice. The material contained carbohydrate, protein, lipid, phosphorus, and 2-keto-3-deoxyoctonate, but no nucleic acid. The beta-hydroxymyristic acid was absent. Results imply that M elsdenii endotoxin has many biological and chemical characteristics common to enterobacterial endotoxin. However, the median lethal doses in mice and in chicken embryos, and minimal dose required to elicit a local Shwartzman reaction, indicate that M elsdenii endotoxin's potency is low, which may explain why the large gram-negative bacterial population in the rumen of cattle is generally innocuous.