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Am J Physiol Gastrointest Liver Physiol 291: G373-G381, 2006. First published June 15, 2006; doi:10.1152/ajpgi.00440.2005
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TRANSLATIONAL PHYSIOLOGY

Interorgan ammonia, glutamate, and glutamine trafficking in pigs with acute liver failure

Lars M. Ytrebø,1 Sambit Sen,2 Christopher Rose,3 Gabrie A. M. Ten Have,4 Nathan A. Davies,2 Stephen Hodges,2 Geir I. Nedredal,1 Manuel Romero-Gomez,5 Roger Williams,2 Arthur Revhaug,1 Rajiv Jalan,2 and Nicolaas E. P. Deutz4

1Department of Digestive Surgery, University Hospital Northern Norway, Tromsø, Norway; 2Liver Failure Group, The University College London Institute of Hepatology, University College London, London, United Kingdom; 3Department of Cellular Neuroscience, Max-Delbrück Center for Molecular Medicine, Berlin, Germany; 4Department of Surgery, Maastricht University, Maastricht, The Netherlands; and 5Hepatology Unit, Hospital Univeritario de Valme, Sevilla, Spain

Submitted 19 September 2005 ; accepted in final form 27 February 2006

ABSTRACT

Ammonia reduction is the target for therapy of hepatic encephalopathy, but lack of quantitative data about how the individual organs handle ammonia limits our ability to develop novel therapeutic strategies. The study aims were to evaluate interorgan ammonia metabolism quantitatively in a devascularized pig model of acute liver failure (ALF). Ammonia and amino acid fluxes were measured across the portal drained viscera (PDV), kidneys, hind leg, and lungs in ALF pigs. ALF pigs developed hyperammonemia and increased glutamine levels, whereas glutamate levels were decreased. PDV contributed to the hyperammonemic state mainly through increased shunting and not as a result of increased glutamine breakdown. The kidneys were quantitatively as important as PDV in systemic ammonia release, whereas muscle took up ammonia. Data suggest that the lungs are able to remove ammonia from the circulation during the initial stage of ALF. Our study provides new data supporting the concept of glutamate deficiency in a pig model of ALF. Furthermore, the kidneys are quantitatively as important as PDV in ammonia production, and the muscles play an important role in ammonia removal.

amino acids; hyperammonemia; hepatic failure; urea cycle


Address for reprint requests and other correspondence: R. Jalan, Liver Failure Group, Institute of Hepatology, Univ. College London, 69–75 Chenies Mews, London WC1E 6HX, UK (e-mail: r.jalan{at}ucl.ac.uk)






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