Superoxide radical involvement in the pathogenesis of burn shock.
The pathogenesis of burn shock syndrome involves the production of superoxide radicals which are first generated in the burned skin. They are responsible for an increase in vascular permeability with loss of plasma, which results in hemoconcentration and hypovolemia. The resulting systemic hypoperfusion leads to a generalized production of superoxide radicals and subsequent cellular damage. Prior administration of allopurinol or superoxide dismutase increases the survival rates of mice subjected to burn shock.
D000493:Allopurinol / Q000627:therapeutic use; D000818:Animals; D002056:Burns / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D005260:Female; D005609:Free Radicals; D006400:Hematocrit; D006439:Hemodynamics; D051379:Mice; D010858:Pigmentation; D012769:Shock / Q000209:etiology / Q000401:mortality / Q000503:physiopathology*; D013482:Superoxide Dismutase / Q000627:therapeutic use; D013481:Superoxides / Q000378:metabolism*; D001743:Urinary Bladder / Q000473:pathology
D005609:Free Radicals; D013481:Superoxides; D000493:Allopurinol; D013482:Superoxide Dismutase