Random flaps can be used to repair wounds and improve shape and functional reconstruction, but inflammation and necrosis limit their application. Modified McFarlane flap models were constructed on the backs of rats. We hypothesized that dexmedetomidine (DEX) could improve the survival rate of ischemic random flaps.

Sixty rats were randomly divided into three groups: a low-dose DEX group (DEX-L group, 10 μg/kg/D), a high-dose DEX group (DEX-H group, 20 μg/kg/D) and a control group (0.9 % saline equivalent). On day 7 after flap construction, the survival percentage of the flap model was calculated. Hematoxylin and eosin staining (H&E) was used to evaluate the histopathological status of the flaps and microvessel density (MVD). Lead oxide/gelatin angiography was used to detect angiogenesis, and laser Doppler flow imaging (LDF) was used to detect blood perfusion. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in the middle areas of the flaps were measured to show the level of oxidative stress. The expressions of Toll-like receptor (TLR4), nuclear factor-kappa B (NF-κB), interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α) and vascular endothelial growth factor (VEGF) were detected by immunohistochemistry.

DEX significantly increased the average survival percentage of the flaps and reduced ischemia and necrosis of the distal end of the flaps. SOD activity significantly increased, while MDA significantly decreased, indicating that DEX reduces oxidative damage. The expression of inflammatory immunoregulatory proteins (TLR4, NF-κB) was downregulated, and the levels of inflammatory factors (IL-1β, IL-6 and TNF-α) were lower. In addition, DEX upregulated VEGF expression, promoted angiogenesis, and increased blood perfusion.

In random flap transplantation, a high dose of DEX is beneficial to flap survival.