Effect of burn injury on glucose and nitrogen metabolism in the liver: Preliminary studies in a perfused liver system

Background. The direct impact of burn injury on liver metabolism was studied in a rat liver perfusion system to remove the influence of systemic factors that modulate liver metabolism. Methods. Seven animals received a barn injury covering 20% of the total body surface area, and seven were sham burned. The in situ liver perfusion studies were carried out in these animals after 3 days of isonitrogenous-isocaloric enteral feeding. In each study oxygen consumption and the rates of uptake and release of glucose, urea, and various amino acids were measured. Results. Burn injury significantly inn-eased urea production (18.5 +/- 0.4 versus 12.2 +/- 0.6 mu mol/gm liver/hr and oxygen consumption (3.23 +/- 0.17 versus 1.21 +/- 0.03 mu mol/gm liver/min) in the liver bat did not alter the rate of gluconeogenesis. The change in amino acid concentrations in the perfusion medium implies an increased net protein breakdown. Conclusions. Our study indicates that (I) burn injury induces a hypermetabolic state in the liver, (2) the observed enhancement of gluconeogenesis in vivo after barn is probably regulated by factors outside the liver, and (3) the liver itself plays an active role in up-regulating urea production in barn injury. Identifying intrahepatic factors that up-regulate urea production may provide an ''intrahepatic approach'' to ameliorate the severe nitrogen loss after burn injury.