Necrosis in TRAM (transverse rectus abdominis myocutaneous) still occurs in flap breast reconstruction. Blood flow may be improved by vascular endothelial growth factor (VEGF), an endogenous protein that stimulates neovascularization. Experimental studies of gene therapy with plasmid vector expressing human VEGF (hVEGF) presented inadequate results. Low level of gene expression could be the cause. To prove that high level of VEGF gene expression can minimize necrosis of TRAM flap, electroporation of VEGF plasmid was tested.
Forty-two adult, male, Wistar-EPM rats were randomly distributed in 6 groups of 7 animals and 50 μg of vectors were injected in the intradermal layer of TRAM flap donor region, by electroporation: LacZ (beta-galactosidase gene); CG (no substance injected and flap elevated); P2G (empty gT plasmid in area 2); PV2G (gT-VEGF165 in area 2); P4G (empty gT plasmid in area 4); PV4G (gT-VEGF165 in area 4). Five days after flap elevation, the animals were euthanized and the degree of necrosis was analyzed by histology and paper template method.
Dermal X-gal staining after electroporation with pSV2lacZ proved high rate of gene transfer. Mean values of necrosis by the paper template method were: CG (74.5%), P2G (62.2%), PV2G (41.1%), P4G (76.6%), and PV4G (59%). Degree of necrosis, preservation of muscle layer, and degree of infiltrates seen by histology were in accordance with mean values of necrosis.
Intradermal injection of gT-VEGF165 in area 2, by electroporation, was effective in reducing unipedicle TRAM flap necrosis, in rats.
