[Disturbed cellular energy metabolism in burns. Studies of rat liver]

Early and adequate shock treatment combined with improved systemic and local therapy practically eliminated primary death of patients with severe burns. In contrast the late mortality, i.e. the fatal outcome during the "burn disease" has not been significantly improved during the last decade. A burn toxin has been discussed as reason of this burn disease. Such a toxic factor has been isolated from burnt mouse and human skin and from the serum of burnt patients as well. Electron microscopic studies in rats revealed similar and comparable mitochondrial alterations of hepatocytes after either a sublethal controlled burn injury or an i.p. application of an equivalent dose of this cutaneous burn toxin. These alterations were dose-dependent. Studies of the liver metabolism of these rats (i.e. gluconeogenesis, urea synthesis and energy metabolism) suggested an inhibited oxidative phosphorylation. Incubation of enzymatically isolated hepatocytes with toxin demonstrated a direct cytotoxic effect of the burn toxin by scanning electron microscopy. Glycogen synthesis and urea synthesis were significantly reduced, hormonal sensibility was partially abolished. These results suggest a disturbance of the cellular energy metabolism via a cell membrane damage. This could be the reason of the decreased host defence of burned patients which causes the fatal outcome in severe burns. Therefore, elimination of burn toxin should be an important point in burn treatment.