作者: Bekir Atik , Önder Tan , Haluk Dülger , Burhan Köseoğlu , Mehmet Bekerecioğlu
DOI: 10.29333/EJGM/82162
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摘要: Burn injury is accompanied by complex pathophysiological alterations that exert deleterious effects on various organ systems (1). Inflammatory shock mediators are implicated in the pathogenesis of burn include histamine, serotonin, kinins, oxygen free radicals (OFR), prostaglandins, thromboxane and interleukins (2). There also experimental evidence documenting superoxide radical involvement (3). Harmful metabolites (O