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Thermal injury in animals and human beings is associated with a series of complications, including susceptibility to bacterial infections and injury to major organs including lung, liver, and kidney. Recent evidence suggests that complement activation associated with burn injury is related to the production of chemotactic peptides, which cause stimulation of circulating neutrophils. Activation of neutrophils leads to the production of hydrogen peroxide and its conversion to toxic products. Iron plays a key role in injury to the lung, either through conversion of H2O2 to hydroxyl radical or through production of the perfenyl ion. It may be that defects in phagocytic cells are due either' to down-regulation or autotoxicity associated with oxygen products. The results of studies on rats indicate that chemotactic peptides stimulate neutrophils in ways that cause autotoxicity, which is catalase dependent and iron dependent, and suggest that activation of mediator systems leads indirectly to injury of tissues and organs beyond the area of thermal trauma.