Activation of TRPV4 Increases Neovascularization of Rat Prefabricated Flaps.

摘要: Background Inadequate neovascularization is a major risk factor that can lead to subsequent necrosis of prefabricated flaps. Recent evidence indicates transient receptor potential cation channel, subfamily V, member 4 (TRPV4) activates growth and remodeling collateral arteries in ischemia tissues by responding elevated fluid shear stress (FSS). Therefore, we evaluated whether TRPV4 could increase flaps rat model. Methods Rat skin were created ligating the right femoral vascular pedicle implanting it underneath abdominal Thirty-six male Sprague–Dawley rats randomly assigned three groups with different solutions injected subcutaneously implantation site around pedicle: normal saline as control group; 4α-Phorbol 12,13-didecanoate (4αPDD), specific activator, 4αPDD or ruthenium red (RR), TRPV-blocker, RR group. Neovascularization was laser speckle contrast imaging (FLPI), histological staining, enzyme-linked immunosorbent assay (ELISA) within two weeks. Afterwards, island completely sutured back. The flap viability survival area examined on day 7. Results A larger survival, higher capillary densities, von Willebrand (vWF) expression observed group comparison those other groups. secretion endothelial (VEGF), but not basic fibroblast (bFGF), significantly Conclusion Activation using via inducement, possibly through VEGF enhancement. serves therapeutic target