Abstract

Ischemic necrosis has been most dreaded complication of flap reconstruction. Therefore, researchers have tried to improvise modalities to prevent or treat it since the onset of flap surgery. So far these researches have failed to identify a pharmacological therapy equally effective as surgical delay in augmenting skin flap viability. In the path of search for this substance, dipyridamole attracted our attention as an antiaggregant agent. Put together with pathophysiological mechanisms underlying ischemic flap necrosis, we concluded dipyridamole might have beneficial effect on survival of skin flaps. In this research random pattern dorsal rat skin flap model of McFarlane is used. Subjects are separated in a randomized fashion between two groups. Experiment group is given dipyridamole with a dose of 20 mg/kg twice daily. Control group is given same amount of saline. At seventh day viability of skin flaps is assessed and compared between groups. Also on 7th day, pathologic specimens are obtained and evaluated histopathologically in terms of neutrophil and lymphocyte infiltration, edema and fibrosis. Necrosis percentage in experiment group is found to be significantly lower than that of control group (p < 0.01*). Neutrophil infiltration and edema found to be significantly lower in dipyridamole group (p < 0.05*). No significant difference is observed in lymphocyte infiltration and fibrosis. Dipyridamole is shown in this research to be effective in augmenting viability of random pattern skin flaps in rats. Nevertheless, more extensive researches are needed to fully determine its precise mechanism, side effects and appropriate doses.

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