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ABSTRACT
Background: Induction of angiogenesis has been shown to be mediated by a number of glycoproteins called growth factors. Growth factors control the growth, differentiation, and metabolism of cells. Vascular endothelial growth factor (VEGF) is believed to be the most potent regulator of this process. The effect of its exogenous administration on the distal third of a long random skin flap was examined. Materials and Methods: Eighteen Wistar rats were divided into two groups of nine. Rats were anesthetized, and a skin flap, measuring 1.5 × 7.5 cm, was elevated at their dorsum. The flap was standardized by centering the pedicle between the lower angles of the scapulae and by using a frame with the previously mentioned dimensions. The length of the flap was five times greater than its width. In group A (n = 9), the flap was elevated, one milliliter of normal saline was injected subdermally, at the distal third, and it was sutured back at its original place. In group B (n = 9), the flap was elevated, injections of 10 μg of VEGF were administrated subdermally, at the distal third, and it was again sutured back. Rats were euthanized a week later and flaps were excised. All specimens were measured, photographed, put in formalin 10%, and were sent for image and histological analysis. Image analysis was used both for the estimation of viable area and for the calculation of mean vessel density per mm2. Results: Necrotic areas of the flaps were clearly demarcated within a week's time. In group A, the mean flap survival percentage was 38.9%. In group B, the percentage was 80.4%. Histological analysis demonstrated angiogenesis in group B, with mean vessel density per mm2 being higher in group B than in group A. Conclusions: Administration of VEGF injections at the distal part of a long random skin flap (length to width ratio 5:1) has been shown to improve the survival rate of the flap and thus contributing to the salvage of greater peripheral segment of the flap. Neovascularization induced by exogenous VEGF seems to be the biological mechanism, which leads to the improvement of flap survival.