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Thermal injury causes directly a liberation of inositolphosphates, diacylglycerols, free arachidonic acid, and lyso PAF from eukaryotic cells. From lyso PAF derivates PAF, from free arachidonic acid are derivating PG, LT, and TX. These "soluble mediators" are stimulating inflammatory cell populations in a feedback mechanism: the stimulus activates the inflammatory cells to produce the same soluble mediators (Fig.1). The arising soluble mediators are the take off for the inflammation cascade causing as later step the activation of kinin, clotting, and complement systems. The pure biochemical lesions at the onset results in the clinical manifestation of oedema, increased dermal temperature, and pains. The possibilities for prevention and allevation of early pain, due to the acute burn, lie in the inhibition of the spreading out of inflammatory mediators (Bauer 1987a) (Fig.2).
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