Desmopressin enhances random-pattern skin flap survival in rats: Possible role of vasopressin Type-1a and 2 receptors

Background: Many drugs have been explored for their role in improving skin flap survival. 1-deamino-8-D-arginine vasopressin (DDAVP or desmopressin) is a synthesized form of anti-diuretic hormone (ADH) and a selective agonist for vasopressin type-2 receptors (V2 receptors). Desmopressin has been shown to improve endothelial function, induce vasodilation, and reduce inflammation. We aimed to evaluate its efficacy in enhancing flap survival and assess the role of vasopressin receptors in this process.Materials and methods: We randomly assigned six male Wistar rats to each study group. Different doses of desmopressin were injected intraperitoneally to find the most effective amount (8 mu g/rat). SR-49059, a selective V1a receptor antagonist, was given at 2 mu g/rat before providing the most effective dose of desmopressin (8 mu g/rat). Histopathological assessments, quantitative measurements of interleukin-1 beta (IL-1 beta), Tumor necrosis factor-alpha (TNF-alpha), and Nuclear Factor-kappa B (NF-kappa B), optical imaging, and measurement of the expression levels of V2 receptor in the rat skin tissue were performed. Results: Desmopressin (8 mu g/rat) significantly reduced the mean percentage of necrotic area compared to the control group (19.35% vs 73.57%). Histopathological evaluations revealed a notable reduction in tissue inflammation, edema, and degeneration following administration of desmopressin (8). The expression of the V2 receptor was increased following desmopressin administration. It also led to a reduction in IL-1 beta, TNF-alpha, and NF kappa B levels. The protective effect of desmopressin on flap survival was reversed upon giving SR-49059. The optical imaging revealed enhanced blood flow in the desmopressin group compared to the control group.Conclusions: Desmopressin could be repurposed to improve flap survival. V1a and V2 receptors probably mediate this effect.