ORIGIN AND FATE OF RUMINAL AMMONIA - A LI TERATURE SURVEY .2. ABSORPTION AND SUBSEQUENT FATE - AMMONIA POISONING

Ruminal ammonia that is not transferred within the liquid phase toward s the omasum or used through microbial proteosynthesis is partly (17 - 51 %) absorbed. Such an absorption depends on the ruminal concentrati on in unionized ammonia which in turn is dependent on the ruminal pH. During absorption, ammonia is partly used through glutamate and glutam ine synthesis within the epithelium. Residual amounts of absorbed ammo nia are then transferred within portal blood to the liver. In this org an, blood ammonia is converted into some metabolites: urea, orotic aci d and probably glutamine. Nevertheless, urea is the main fate of blood ammonia in ruminants. From 60 up to 80% of the hepatic urea productio n arises from absorbed ammonia, the exceeding part coming mainly from the catabolism of amino acids that are not used through body proteosyn thesis. Urea follows two pathways to leave the blood compartment: the urinary excretion and the transfer into the lumen of the digestive tra ct (DT), 90 % of the hepatic urea production following the second rout e when ingested amounts of nitrogenous compounds are very low. (1) Uri nary urea amounts depend not only on the blood urea level but also on the glomerular filtration and tubular reabsorption rates of that metab olite. (2) Urea transfert into the DT is dependent on the alimentary e nergy and nitrogen supplies and also on the physiological state of the ruminant. Because of the ruminal recycling of endogenous urea, such a transfert does benefit to the animal when it takes place in the rumen . Blood urea reaches that forestomach with saliva and/or by diffusion across the rumen wall. (1) Salivary urea amounts depend on the salivar y secretion rate and on the blood urea concentration. (2) Whereas urea passage across the epithelium is enhanced by high ruminal concentrati ons in CO2 and in butyric acid, such a process is inhibited by high ru minal ammonia levels. To conclude, ruminal ammonia is an important met abolite of nitrogen (N) metabolism in ruminants. On the one hand, it p lays a central role in the digestive utilization of nitrogenous compou nds: ruminal ammonia is both the ultimate metabolite to be produced th rough the breakdown of nitrogenous compounds and a major nutrient in b acterial proteosynthesis. On the other hand, it plays a role in a surv ival mechanism as endogenous urea-N recycling which mainly occurs when N supplies are very low. Nevertheless, excessive ammonia release in t he rumen participates to a ruminal pH increase which in turn enhances ammonia absorption and therefore leads to an increase in blood ammonia concentration. As a result, ammonia poisoning may take place. This oc curs when blood ammonia level reaches 5 - 10 mg/l and may lead to the loss of the ruminant. Such an event is observed when ruminal ammonia l evel is around 1,700 mg/l, an ammonia concentration of 400 mg/l distur bing already the reticulo-rumen motility.