The Effects of Deferoxamine on the Oxygen Free Radical and Neutrophil in Ischemia-Reperfusion Injury.
- Author:
Gyeol YOO
1
;
Seung Hyun HONG
;
Sung Shin WEE
;
Sang Hoon CHUNG
;
Ki Taek HAN
Author Information
1. Department of Plastic & Reconstructive Surgery, College of Medicine, The Catholic University of Korea, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Ischemia-reperfusion injury;
Oxygen free radical;
Neutrophil;
Deferoxamine
- MeSH:
Abdomen;
Animals;
Deferoxamine*;
Free Radicals;
Iron;
Membranes;
Necrosis;
Neutrophils*;
Oxygen*;
Phospholipids;
Rats;
Reperfusion;
Reperfusion Injury*;
Skin;
Survival Rate
- From:Journal of the Korean Society of Plastic and Reconstructive Surgeons
2000;27(3):270-275
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Adequate circulation is indispensable for flap survival. Ischemia-reperfusion injury is one of the causes of flap necrosis. Current evidence suggests that tissue damage associated with ischemia-reperfusion injury and inflammatory responses may be mediated by oxygen free radicals and neutrophils. Oxygen free radicals can directly alter structural component of tissue, attack membrane phospholipids and produce the chemotactic factor for neutrophil which is main cell in inflammatory reactions and an important source of oxygen free radicals. Deferoxamine is well known as a powerful chelator of iron and free radical scavenger. It is also known to decrease the skin flap necrosis. The purpose of this study is to evaluate the effects of deferoxamine on the oxygen free radicals and neutrophils after ischemia-reperfusion injury of skin flaps. A 6 x 3 cm sized island skin flap was made on the left abdomen of rat and the epigastric pedicle was occluded for 6 hours. Thirty minutes before reperfusion, the flaps were perfused with normal saline or deferoxamine. The flap survival rates were assessed by computerized planimetry on the fifth day after reperfusion. Tissues for assay of MDA and MPO were obtained at 6, 12, 24, 48 hours after reperfusion. The results were as follows: 1. Deferoxamine administration groups improved flap survival rates significantly compared to control groups (78.3+/-13.2%, 54.6+/-6.35%) (p = 0.0011). 2. The level of MDA was significantly lowered in deferoxamine administration groups compared to control groups(p<0.05). The levels of MDA were increased over time in each group but, the ircrement was steeper in control groups than that in deferoxamine administration groups. In control groups, the increment between 6 and 12 hours was argest. 3. MPO content was increased over time in each group but significantly low in deferoxamine administration groups compared to control groups(p<0.05). The increment of control groups was steeper than that of deferoxamine administration groups. We conclude that deferoxamine improve the flap survival rates after reperfusion injury by inhibition of production of oxygen free radicals and neutrophil influx via a free radical scavenger 8 anti-inflammatory action.
