Evaluation of random skin flap survival in a porcine model

The pathophysiology of random skin flap necrosis in the pig model was studied the effects of several drugs on skin flap survival were examined. The investigated drugs included acetylsalicylic acid (ASA), pentoxifylline (PTX), prostaglandin E(2) (PGE(2)), and an experimental 21-aminosteroid, U-74389G. Each drug altered different parameters known to be associated with tissue necrosis. Demonstrated mechanisms of skin nap failure included the alteration of erythrocyte flexibility and platelet function and the activation of neutrophils with resultant accumulation of damaging oxygen-free radicals. Random skin nap survival did not improve with ASA but did improve significantly with PTX, PGE(2), and U-74389G. The results of this study underscore the importance of neutrophil-mediated necrosis in the pathophysiology of skin flap failure. The data further demonstrate the need to develop drugs aimed at reversing or preventing the tissue damage from oxygen-free radicals in order to enhance the survival of random skin naps.