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

@entity1 @entity66 @entity1133 @entity19 @entity4808 @entity35
Early and adequate shock treatment combined with improved systemic and local therapy practically eliminated primary death of @entity1 with severe burns. In contrast the late mortality, i.e. the fatal outcome during the " @entity66 " has not been significantly improved during the last decade. A burn toxin has been discussed as reason of this @entity66 . Such a toxic factor has been isolated from burnt @entity19 and @entity1 skin and from the serum of burnt @entity1 as well. Electron microscopic studies in @entity35 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 @entity35 (i.e. gluconeogenesis, @entity1133 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 @entity1133 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 @entity4808 @entity1 which causes the fatal outcome in severe burns. Therefore, elimination of burn toxin should be an important point in burn treatment.
