Aliskiren promotes skin-flap survival

Flaps are used in clinical wound repair, reconstruction, and plastic surgery but are prone to necrosis after surgery. Aliskiren, a direct renin inhibitor, may promote flap survival. Thirty-eight rats were divided into control and low- and high-dose aliskiren groups (n = 12 rats per group; two rats in the high-dose group died and were replaced). The flap survival rate, neutrophil density, microvessel density, superoxide dismutase activity, and malondialdehyde level were evaluated, and histopathological analysis was performed, on day 7 after surgery. Blood perfusion was measured by laser Doppler flowmetry and oxide-gelatin angiography. The levels of vascular endothelial growth factor, tumor necrosis factor-α, interleukin (IL)-6, Nod-like receptor 3, cysteinyl aspartate specific proteinase-1 (caspase-1), IL-1β, and IL-18 were evaluated by immunohistochemical analysis. Aliskiren improved flap survival. Downregulation of the malondialdehyde level and upregulation of the superoxide dismutase level in the experimental groups suggested that aliskiren reduced ischemia–reperfusion injury. Upregulation of the vascular endothelial growth factor level and improvement of blood perfusion in the experimental groups suggested that aliskiren improved flap angiogenesis. Immunohistochemical analysis showed that aliskiren reduced the levels of inflammatory factors such as tumor necrosis factor-α and IL-6. Furthermore, the expression of Nod-like receptor 3 inflammasome components was decreased in the experimental groups. Aliskiren improved the flap-survival rate.