Human skin is known to be able to metabolize arachidonic acid into prostaglandins and thromboxanes. This metabolism can be activated by any inflammatory stimulus such as a burn. In burn patients, the production of prostaglandin and thromboxane is proven to aggravate the pathological process due to impairment of the microcirculation of skin by formation of thrombosis.
It has been reported that prostaglandins E and F have been isolated from human burn blisterfluid. There has been increasing recognition in the recent literature that immunoregulatory factors can often be detected in the serum of patients with thermal and traumatic injuries are profoundly immunosuppressed. The agent that suppress the immune response in serum can be easily detected using in vitro lymphocyte assays. Now it is known that burn toxin complex(PGE?＋endotoxin) causes the immune suppression.
In the present experiment, the toxic effects of burn exudate, conjugating postaglandins (PGE?, PGF?α) and prostaglandin synthesis inhibitors(acetyl salicylic acid, indoprofen, flurbiprofen) were observed and the following results were obtained:
1. The amount of protein in the burn exudates was significantly higher than in the nonspecific inflammatory exudates as well as the control exudates,
2. The toxic effect was significantly increased when the burn exudates were given to mice compaired with the other exudates (nonspecific inflammation, control)
3. When the prostaglandin synthesis inhibitors were administered, no significant differences on the toxic effects were observed between the burn exudates and control exudates.
4. However, at 5 days following the administration of PG synthesis inhibitors the toxic effects of burn exudates became evident (mortality rate 30.6%).
5. The toxic response of PGF?αdid not change with increased dosage, but the toxic response of PGE? was aggravated by increased dosage.
6. On histologic examination, the liver and kidney showed hemorrhage and cong estion. Focal necrosis was seen around the central vein of the liver and amount of kupffer cell was increased.
In conclusion it can be said that the burn exudate (burn toxin) produced from the burned skin should be composed of prostaglandin, especially PGE?.
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