Abstract
Evidence suggests that failure of flap reconstruction is related to ischemia/reperfusion (I/R)-mediated endothelial damage. Using a rat inferior epigastric artery flap as an I/R injury model, we investigated whether administration of nitrosoglutathione (GSNO), an exogenous nitric oxide (NO) donor, can scavenge superoxide and promote flap survival. Thirty minutes before flap reperfusion, normal saline, N-acetylcysteine (75 and 150 mg/kg), or GSNO (0.2 and 0.6 mg/kg) was randomly injected into 10 rats. Superoxide, nuclear factor-kappa B (NF-kappa B) activation, NO synthase (NOS) isoforms, and 3-nitrotyrosine expression in the pedicle vessels as well as survival areas of the flaps were evaluated. I/R injury induced superoxide production, NF-kappa B activation, and inducible NOS (iNOS) expression in the pedicle vessels. GSNO significantly inhibited superoxide production and suppressed NF-kappa B activation, iNOS induction, and 3-nitrotyrosine expression, but up-regulated endothelial NOS expression in the flap vessels. Optimal doses of both GSNO (0.6 mg/kg) and N-acetylcysteine (150 mg/kg) effectively promoted flap survival area (p < 0.001), although there was no significant difference between both groups. Exogenous NO donation by GSNO can scavenge superoxide and suppress iNOS induction, resulting in better flap survival after prolonged ischemia.
Published Version
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