Antioxidant Treatment in Experimental Thermal Injury
There is increasing experimental evidence to suggest that oxygen-derived free radicals play an important role in the pathophysiology of thermal injury. Following thermal injury of skin, oxygen radicals have been linked to the appearance of lipid peroxidation products (1–3) and the pathogenesis of burn shock (4). Experimental studies have shown that edema formation in the skin of rats following a partialthickness burn is mainly mediated by oxidants derived from xanthine oxidase (5, 6). In addition, there is evidence that the development of intravascular hemolysis and acute lung injury secondary to thermal trauma can be linked to the generation of oxygen radicals from complement-activated blood neutrophils (7, 8). In these model systems of thermal injury, antioxidant interventions have demonstrated pronounced, protective effects supporting the concept that oxygen radicals are playing an important role in local as well as distant cell and tissue damage following thermal injury.
KeywordsAcute Lung Injury Xanthine Oxidase Thermal Injury Lipid Peroxidation Product Edema Formation
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- 5.Till GO, Guilds LS, Mahrougui M, Friedl HP, Trentz 0, Ward PA: Role of xanthine oxidase in thermal injury of skin. Am J Pathol 1989, in press.Google Scholar
- 6.Friedl HP, Till GO, Trentz O, Ward PA: Roles of histamine, complement and xanthine oxidase in thermal injury of skin. Am. J. Pathol. 1989, in press.Google Scholar
- 11.Rocha E, Silva M, Antonio A: Release of bradykinin and the mechanism of production of thermic edema (45°C) in the rats paw. Med Exp 1960, 3:371–382.Google Scholar