Comparison of the effects of different vasoactive and antiplatelet drugs on perforator flap viability. An experimental study

Abstract

Perforator flaps are very popular in the reconstruction of soft tissue defects. As these flaps generally depend on a single perforator, drugs that increase the perfusion of the flap and/or prevent vascular complications may increase flap survival. In this study, we compared the effects of systemically administered hydralazine (arterial vasodilator via potassium channels), nifedipine (arterial vasodilator via calcium channels), piracetam (antiplatelet and regulator of microcirculation) and alprostadil (vasodilator, antiplatelet, rheological and cytoprotective) on flap survival in a rat epigastric artery perforator flap model. The percentage of necrosis was measured on each flap and evaluated using one-way analysis of variance (Anova). Histopathological analyses were also performed. Mean flap survival area was 3.85 cm2 in the control group. Mean flap survival area was 4.88 cm2 in the nifedipine group, 4.69 cm2 in the hydralazine group, 10.55 cm2 in the piracetam group and 11.3 cm2 in the alprostadil group. When compared with the control group, all drugs except hydralazine improved flap survival; piracetam and alprostadil yielded significantly better results than nifedipine. Only the alprostadil group showed signs of improved vascularity in the histological analysis. As far as perforator flap survival is concerned, drugs that regulate the microcirculation by a combination of different antiaggregation mechanisms appear more beneficial than single action vasodilators. Alprostadil, a synthetic PGE-1 analogue, has combined antiplatelet and vasoactive effects that further increase flap survival.