Maintaining the viability of an extended skin flap remains one of the
continuing challenges in reconstructive surgery. As flaps lengthen, vi
ability 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. Vasod
ilators 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 pro
perties. A standard rat flap model was used to help clarify the potent
ial of nifedipine to salvage ischemic skin flaps. Alterations in flap
perfusion were assessed using a laser Doppler flowmeter and dermofluor
ometry in an attempt to characterize nifedipine's mechanism of action
on flap preservation. Increased flap survival was demonstrated in trea
tment animals when compared to controls. Despite significant improveme
nt in flap viability, perfusion measurements failed to confirm increas
ed flow within the flap microcirculation. Although the mechanisms of a
ction remain speculative, nifedipine may have important therapeutic po
tential in improving skin flap survival in a clinical setting.