Maintaining the viability of an extended skin flap remains one of the continuing challenges in reconstructive surgery. As flaps lengthen, viability becomes more unpredictable and necrosis of distal segments can occur. The specific mechanisms involved in determining flap survival remain unclear, but vasoconstriction within the flap microcirculation appears to play a significant role in regulating flap viability. Vasodilators have been used, with limited success, in an attempt to improve survival of ischemic skin flaps in rats. One such agent, nifedipine, a calcium channel blocker, demonstrated conflicting results when used to improve rat skin flap survival, despite its potent vasodilating properties. A standard rat flap model was used to help clarify the potential of nifedipine to salvage ischemic skin flaps. Alterations in flap perfusion were assessed using a laser Doppler flowmeter and dermofluorometry in an attempt to characterize nifedipine's mechanism of action on flap preservation. Increased flap survival was demonstrated in treatment animals when compared to controls. Despite significant improvement in flap viability, perfusion measurements failed to confirm increased flow within the flap microcirculation. Although the mechanisms of action remain speculative, nifedipine may have important therapeutic potential in improving skin flap survival in a clinical setting.