Effect of colectomy upon ammonemia and glutaminemia in rats with stricture of the portal vein.
Current theories on the pathogenesis of hepatic encephalopathy indicate that intestinal bacteria produce cerebral toxins, such as ammonia; colectomy has been proposed in the treatment of chronic portal systemic encephalopathy. This study was undertaken to evaluate the evolution of ammonemia and glutaminemia during a four month period in rats after a colectomy, with and without portal vein stricture. Groups of nine rats were studied: group 1 served as control study, total colectomy was performed on the rats in groups 2 and 3, but a gradual stricture of the portal vein was produced in the rats of group 3 and group 4 that had not had a colectomy. The ammonia levels were stable in groups 1 and 2, 48 +/- 2 milligrams per 100 milliliters; in group 3, ammonia levels rose significantly one week after portal vein stricture, 136 +/- 10, and decreased progressively until the end of the first month, 70 +/- 10, although in group 4 of the ammonia level always remained higher than in this one. The levels of glutamine decreased after colectomy in group 2 and rose markedly in both groups 3 and 4 during the first week but persisted at the same level only in group 4. These data confirm the importance of hepatic clearing of portal blood in ammonia and glutamine metabolism and underline the importance of the colon as the main, but not exclusive, site of splanchnic ammonia and glutamine production. The improvement in hepatic encephalopathy observed after removal of the colon may be due to the reduced output of these two substances.
D000641:Ammonia / Q000097:blood*; D000818:Animals; D003082:Colectomy; D003251:Constriction, Pathologic; D005973:Glutamine / Q000097:blood*; D006501:Hepatic Encephalopathy / Q000097:blood / Q000209:etiology / Q000601:surgery*; D008297:Male; D011169:Portal Vein; D051381:Rats
D005973:Glutamine; D000641:Ammonia