Montelukast protects axial pattern rat skin flaps against ischemia/reperfusion injury.
BACKGROUND
Recent studies have shown that neutrophils play an important role in the pathogenesis of reperfusion injury. Using an inferior epigastric artery skin flap as a flap ischemia/reperfusion (I/R) injury model, we investigated whether the administration of montelukast sodium, a selective reversible cysteinyl leukotriene 1 (CysLT1) receptor antagonist, decreases neutrophil infiltration and promotes flap survival.


METHODS
Eighteen rats were used and randomly divided into three groups (n=6 for each group). Group I was the sham group and did not undergo ischemic insult; rather, normal saline (1 mL) was administrated intraperitonealy (i.p.) 30 min before surgery and continued for 6 d. Group II (control) and Group III (montelukast) underwent 12 h of ischemic insult. For Group II, normal saline (1 mL) was injected i.p. 30 min before the surgery and immediately before reperfusion, and this continued for 6 d. In Group III, 1 mL of montelukast (10mg/kg) was injected i.p. and continued for 6 d. Malondialdehyde (MDA) and glutathione (GSH) levels and myeloperoxidase (MPO) enzyme activities were investigated. Histological evaluation was made to investigate the tissue neutrophil count. Survival areas were assessed at 7 d postoperatively.


RESULTS
Group III (montelukast- treated) showed a significantly higher survival rate than Group II (control) (P=0.029) but a lower survival rate than Group I (sham). Histological and biochemical assays corroborated this data.


CONCLUSIONS
This study suggests that montelukast CysLT1 receptor antagonist montelukast reversed I/R-induced oxidant responses and improved flap survival by inhibiting neutrophil infiltration and balancing oxidant and antioxidant status.
Gideroglu
Kaan
K
Department of Plastic and Reconstructive Surgery, Abant Izzet Baysal University, Medical Faculty, Bolu, Turkey. kaangideroglu@hotmail.com
Yilmaz
Fahrettin
F
Aksoy
Fadullah
F
Bugdayci
Guler
G
Saglam
Ibrahim
I
Yimaz
Fahri
F
D000085:Acetates / Q000008:administration & dosage / Q000627:therapeutic use*; D000818:Animals; D002465:Cell Movement / Q000502:physiology; D003521:Cyclopropanes; D005978:Glutathione / Q000378:metabolism; D006085:Graft Survival / Q000502:physiology*; D007274:Injections, Intraperitoneal; D020024:Leukotriene Antagonists / Q000008:administration & dosage / Q000627:therapeutic use*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D023421:Models, Animal; D009504:Neutrophils / Q000473:pathology; D009195:Peroxidase / Q000378:metabolism; D011804:Quinolines / Q000008:administration & dosage / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000473:pathology / Q000517:prevention & control*; D016038:Skin Transplantation / Q000473:pathology / Q000502:physiology*; D013440:Sulfides; D013524:Surgical Flaps / Q000473:pathology / Q000502:physiology*; D016896:Treatment Outcome
D000085:Acetates; D003521:Cyclopropanes; D020024:Leukotriene Antagonists; D011804:Quinolines; D013440:Sulfides; D008315:Malondialdehyde; D009195:Peroxidase; D005978:Glutathione; C093875:montelukast