The effect of prostaglandin E1 versus ischemia-reperfusion injury of musculocutaneous flaps

Citation
Jp. Hong et al., The effect of prostaglandin E1 versus ischemia-reperfusion injury of musculocutaneous flaps, ANN PL SURG, 47(3), 2001, pp. 316-321
Citations number
31
Categorie Soggetti
Surgery
Journal title
ANNALS OF PLASTIC SURGERY
ISSN journal
01487043 → ACNP
Volume
47
Issue
3
Year of publication
2001
Pages
316 - 321
Database
ISI
SICI code
0148-7043(200109)47:3<316:TEOPEV>2.0.ZU;2-P
Abstract
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.