OBJECTIVE To investigate the mechanism of necrosis of avulsion injured skin flap. METHODS Six swine were used. An avulsed skin flap and traditional island flap were made on each hind leg of the swine respectively, and the latter was used as control. Then the microvascular casting of each flap was made routinely immediately following the injury and 72 hours later, and the vascular casting were observed under electron microscopic scanning. RESULTS There were three characteristic changes in the avulsed skin flap: tearing of blood vessels, formation of complete thrombosis and incomplete thrombosis. If these changes were excessive in the avulsed flap, then the necrosis was the result, otherwise, the flap survived. CONCLUSION The necrosis of avulsed flap was related to the type and extent of the damage of microvascular endothelial structure. So the degree of endothelial damage was the keypoint in the viability of avulsed flap.
To investigate the function of nitric oxide (NO) and nitric oxide synthetase (NOS) inhibitor, N-nitro-L-arginine methyl ester (L-NAME), the skin avulsion model was made in the lower extremity of pig. The methods of measurement of size of the survived flap, weighing, immunocytochemistry and hybridization in situ were employed, so that the survival surface area of flaps, tissue wet/dry weight ratio, NO content in the serum, gene expression of NO and NOS content in the flap tissue were determined, respectively. The results showed that the early gene expression of NOS was increased as well as the NO content and tissue wet/dry weight ratio (P lt; 0.01). After L-NAME was applied introvenously, the NO content and tissue wet/dry weight ratio were decreased (P lt; 0.01), and the survival surface area of flaps was enlarged (P lt; 0.01). It could be concluded that the NO might play a role in the development of the pathological changes as early congestion, edema and secondary necrosis in the avulsed skin flaps. The early application of L-NAME could do some good to the avulsed skin flap and protect it from further necrosis owing to the presence of NO.