The purpose of this study was to identify the length of the ischaemic
period required to induce the 'no-reflow' phenomenon in a rat epigastr
ic flap on an avascular recipient site. The vascularity of the recipie
nt bed may affect flap survival in the early postischaemic stage after
flap transfer. Initially, we designed epigastric flaps in 300-350 g S
prague-Dawley rats and separated the rats into four groups of 5 rats e
ach (total 20 rats). In groups 1, 2, 3, the flaps were made ischaemic
for 1 hour, 6 hours and 10 hours, respectively, by temporarily clippin
g the epigastric artery and vein. In group 4, the epigastric artery an
d vein were divided to create permanent ischaemia. In groups 1, 2 and
3, ischaemia was ended by removing the clips. After the ischaemic flap
s were reperfused, their viability was studied by measuring the flap s
urvival rate at postoperative day 7. Flap survival was studied by dire
ct observations, laser Doppler flowmeter measurement of flap blood flo
w, histopathology, and carbon particle perfusion of the flap vasculatu
re. Ischaemic flaps of groups 1 and 2 recovered almost completely afte
r reperfusion due to the short period of ischaema.In a second series o
f experiments, in order to evaluate the contribution to flap survival
of the recipient vascularised bed, another four groups of epigastric f
laps (of 5 animals each, using the same time periods as above) were ra
ised and a piece of Biobrane was interposed between the flap and the r
ecipient bed before the flap wound was closed, to eliminate all nutrie
nt supply from the recipient bed. The results showed that the combined
effect of the reperfused flap vasculature plus the metabolic contribu
tion of the recipient bed significantly (P < 0.01) increased the exten
t of flap survival of the 6- and 10-hour ischaemic flaps as well as th
e divided pedicle flaps, which were never reperfused. An absolute 'no-
reflow' rat model flap for further flap salvage studies was also devel
oped.