Abstract. A lipid‐protein complex, which has a lethal effect on recipient animals, was isolated from mouse skin exposed to controlled thermal energy. A new isolation procedure was developed, which takes advantage of the toxic activity present in thermally modified skin, to trace the fate of the active compound. A bioassay was designed for this purpose by injecting Thorotrast into the recipient animals. The toxic lipid‐protein complex and the corresponding derivative from native skin were shown to have the same lipid (40%) and protein (60%) content. The lipid moieties of both derivatives were made up of six different lipid classes. The toxic compound differed from the non‐toxic material only by its larger size and higher density. Equivalent results were obtained on samples isolated, after the removal of surface lipids and soluble cell constituents, from the donor skins prior to the application of thermal energy i.e. processing “skin residues”. The biological activity was shown to reside in the apoprotein while the lipid moiety contributes to the toxic activity to a certain extent. The results suggest that the toxic compound is a polymeric form produced by thermal energy from a naturally occurring precursor. The toxin has a specific antigenic property protecting mice after active and passive immunotherapy against a lethal bum injury in vivo. This suggests strongly that the toxic compound is an etiological factor responsible for the high mortality after severe burns. It is significant that, if scalding was applied to the same extent as the dry heat burns in vivo, the injured animals survived. This was interpreted to support the hypothesis of a specific mechanism being responsible for toxin formation. The experimental results suggest that a specific therapy for the “late mortality” after severe human burns might be possible.
Pathophysiological Studies with a Burn Model in Mice Summary1. A new technique to apply high temperature burns and scalds under controlled conditions in living mice has been established.2. The difference between scalds and high temperature heat injuries with respect to the histological changes, the temperature profile within the skin and the mortality rate has been demonstrated. A mechanism for toxin formation shown to occur in vitro in mammalian skin under standardized energy application was reproduced in vivo.3. The toxic effect of the isolated product and the lethal burn injury (in vivo) upon kidney function measured by serum creatinine and urea has been shown. 4. The relationship between the surface area injured and the animal's body weight and total surface as a critical parameter with respect to the survival chance has been established.
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