Lipid material toxic to mitochondria

Lipid material toxic to mitochondria

376 the allograft. At about 3 weeks this process was complete with a flat epithelium covering the entire wound surface. Gang R. K., Hamberg H., Artur...

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the allograft. At about 3 weeks this process was complete with a flat epithelium covering the entire wound surface. Gang R. K., Hamberg H., Arturson G. et al. (1981) Histological studies of intermingled transplantation of autografts and allografts in rabbits. Burns 8,80. Limitation of operative blood loss Studies in pigs with deep burns (250 “C, I5 seconds) covering about one-third of the body surface receiving lysine vasopressin (1.2 iu per kg body weight) given 30 minutes after burning and then at a constant rate for the next 5 hours showed that this compound limited blood loss during the acute excision of the burned tissue. There was reasonable blood flow to all vital organs and urine volume increased. Vernersson E.. Wetterlin S., Ahlgren I. et al. (1981) Effects of lysine vasopressin on blood loss and haemodynamics after early excision in burned pigs. Burns 8, 131. LABORATORY STUDIES Lipid material toxic to mitochondria Burned skin and eschar tissue contain a lipid substance which is toxic to liver mitochondria. The substance depresses the respiratory control index and the rates of formation of ATP and adenosine diphosphate oxygen complex. The lipid material was found at maximal concentrations l-2 weeks after burning; it is heat stable and can be extracted from tissues with ether. Since the substances can also be found in normal skin in trace amounts, burning injury may produce increased amounts by heat-induced polymerization of fatty acids. Suzuki K., Aoyama H., Izawa Y. et al. (1981) Isolation of a substance toxic to mitochondrial function from the burned skin of rats. Burns 8. I IO. Benefits of early cooling of burned tissue Light and electron microscopy was used to determine

Burns Vol. 8/No. 5

the changes induced by the early (within IO minutes) cooling in ice water of partial-thickness skin loss injury covering IO per cent of the body surface ofguinea-pigs. During the first 24 hours after injury cooling was associated with a reduced loss of epidermis and reduced damage to the basement membrane, There was also less damage to the dermal microvasculature and less oedema fluid compared with untreated burn wounds. At 96 hours, the cooled burn wounds showed minimal dermal haemorrhage and polymorphonuclear leucocyte infiltration compared with the untreated wounds. de Camara D. L., Raine T. and Robson M. C. (198I) Ultrastructural aspects of cooled thermal injury. J. 7-ra~ma21,9ll. Permeability of burned skin The permeability of skin burned at temperatures between 60 “C and 250 “C with a dry branding iron has been tested with water and a series of n-alkanols spanning methanol to octanol. Skin permeability was not impaired uv to 70 “C but then increased dramatically at higher temperatures and with the polar solvents (water, methanol and ethanol). The increase in permeability with respect to temperature was only moderate for butanol. slight for hexanol and virtually unchanged with octanol. The stratum corneum was much more sensitive to the effects of temperature than the dermal barrier when measured with the various n-alkanols. The alkyl chain length sensitivity of permeation diminished linearly with increasing temperature of burning, reaching a value of zero at about I20 “C; this indicated complete loss of the partitioning dependency of the permeation process and therefore functional alteration ofthe strateum corneum. Behl C. R., Flynn G. L., Barrett M. et al. (198 I) Permeabilitv of thermallv damaged skin IV: influence of branding-iron temperature on the mass transfer of water and n-alkanols across hairless mouse skin. Burns 8,86.