The role of inflammatory mediators

The observation of progressive changes in the burn wound suggest the possibility that inflammatory mediators may play a role. Vasoactive mediators such as histamine, prostaglandins, and bradykinin can produce edema by direct action on endothelial cell permeability or indirectly by increasing microvascular hydrostatic pressure. While the role and significance of vasoactive substances and mediators is unclear, the concept of mediator-induced injury takes on clinical importance because of the theoretical possibility of injury modulation by mediator inhibition ( DemlingJ990). Histamine, released either as a direct result of heat or by stimulation of mast cells, is found in increased concentrations after thermal injury. Prevention of histamine release by H 2-blocking agents has been demonstrated to decrease the edema-producing effects of vasodilation and increased microvascular permeability.

The complement system is activated by an undefined mechanism. C5a appears to be the initiating factor in the inflammatory response, activating intravascular neutrophil secretion of histamine. C5a also catalyzes conversion of xanthine dehydrogenase into xanthine oxidase by interacting with endothelial cells leading to formation of oxygen radicals. Full-thickness burns exceeding 20 per cent of body surface area are associated with increased systemic oxidant activity, as measured by increased liver lipid peroxidation. Animal studies have shown that alterations in ATP production can be reversed by treatment with water-soluble antioxidants, suggesting a cause-and-effect relationship (Lalon.d..e...e.i,a/ 1996). C5a may also play a role as a cofactor in the production of tumor necrosis factor-a.

Oxygen free radicals may exert an indirect effect through the release of arachidonic acid metabolites. Prostaglandins released from burn tissue may contribute to edema formation. Moreover, burn injury is associated with increased plasma levels of nitric oxide, a potent endogenous vasodilator ( Preiser..eia[ 1996). This appears to be due to increased release rather than decreased renal clearance. Nitric oxide may also participate in burn-related hemodynamic and immunological alterations.

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