The failing free flap remains a major problem for the reconstructive s
urgeon. Many and varied pharmacologic agents have been utilized to rev
erse the effects of ischemia in these flaps. Treatments have been aime
d at inhibiting presumed causative factors in the no-reflow phenomenon
. Therapy has generally been single in nature and designed to affect o
nly one of these presumed factors. In this study, several pharmacologi
c agents were utilized individually or in combination therapy as posti
schemic washouts, in an effort to attack the multiple causative factor
s in the no-reflow phenomenon and to improve flap survival in a rat ab
dominal skin flap model. The treatment agents included lactated Ringer
's, superoxide dismutase, and urokinase, with each used independently
as a postischemic perfusion washout. Combination therapy utilized an i
nitial postischemic perfusion with urokinase, followed by a second per
fusion washout with superoxide dismutase. After 18 hr of primary ische
mia, there was increased flap survival in the animals undergoing perfu
sion washout with either superoxide dismutase alone or with combined u
rokinase and superoxide dismutase washouts, compared to all other trea
tments (p < 0.001). It was found that flaps undergoing combined urokin
ase and superoxide dismutase postischemic perfusion washouts demonstra
ted significantly improved survival after 20 hr of primary ischemia, c
ompared to all other therapies (p < 0.05). By demonstrating improved s
urvival when a thrombolytic agent is used in conjunction with an oxyge
n free radical scavenger, these Endings may have implications in the t
reatment of clinically failing free flaps.