The purpose of this study was twofold. To evaluate whether prostaglandin E1
can increase the survival of the flap, and to determine its function again
st ischemia-reperfusion injury in musculocutaneous flaps. Thirty-five Sprag
ue-Dawley rats weighing 250 to 350 g were analyzed. The transverse rectus a
bdominis musculocutaneous flap was used in all rats. The rats were divided
into three groups: group 1 (N = 15), the control group with 4-hour ischemic
injury and intraflap injection of normal saline followed by reperfusion; g
roup 2 (N = 15), prostaglandin E1 intraflap injection of 1 mug immediately
after ischemic injury and reperfusion 4 hours later; and group 3 (N = 5), t
he sham-operated group. Analysis consisted of flap skin survival area measu
rements, immunohistochemical study using anti-intercellular adhesion molecu
le (anti-ICAM-1) monoclonal antibody, and histological evaluation including
endothelium-sticking leukocytes at 24 hours and 5 days after reperfusion.
The group treated with prostaglandin E1 showed immunohistochemical findings
with decreased expression of ICAM-1 on the surface of the endothelium, and
histology showed significant (p < 0.01) reduction of leukocyte adhesion at
24 hours and 5 days after reperfusion. These two factors were considered t
o play a role against ischemia-reperfusion injury, and led to improved surv
ival of the flap. These results suggest that prostaglandin E1 may increase
flap survival and may have a protective mechanism against ischemia-reperfus
ion injury by decreasing leukocyte-endothelial cell adhesion through decrea
sed expression of ICAM-1.