Hepatic portal vein ammonia

The ammonia produced from asparagine and glutamine is released into the hepatic portal vein, for removal by the liver and conversion to urea. The concentration of ammonia in the blood in the hepatic portal vein is about ten times higher than in the hepatic vein, indicating the quantitative importance of the liver in removing this ammonia. 

To some extent, humans excrete urea into the gut and saliva. Intestinal bacteria convert urea to ammonia. This ammonia, as well as ammonia produced by other bacterial reactions in the gut, is absorbed into the hepatic portal vein. It is normally extracted by the liver and converted to urea. Approximately one fourth of the total urea released by the liver each day is recycled by bacteria. 

A large fraction of the ammonia that is converted to urea in the liver comes from metabolism in the extra-hepatic tissues, although only a small fraction leaves these tissues as anunonia. The absorptive cells of the small intestine are exceptional in this respect, in that they release anunonia into the portal vein there the anunonia concentration may reach 0.26 mM, accoiuiting for 30% of the urea synthesized in the liver. 

The ammonia produced by enteric bacteria and absorbed into portal venous blood and the ammonia produced by tissues are rapidly removed from circulation by the liver and converted to urea. Only traces (10—20 Ig/dL) thus normally are present in peripheral blood. This is essential, since ammonia is toxic to the central nervous system. Should portal blood bypass the liver, systemic blood ammonia levels may rise to toxic levels. This occurs in severely impaired hepatic function or the development of collateral links between the portal and systemic veins in cirrhosis. Symptoms of ammonia intoxication include tremor, slurred speech, blurred vision, coma, and ultimately death. Ammonia may be toxic to the brain in part because it reacts with a-ketoglutarate to form glutamate. The resulting depleted levels of a-ketoglutarate then impair function of the tricarboxylic acid (TCA) cycle in neurons. 

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