title: Effect of Montelukast on Spinal Cord Ischemia- Reperfusion Injury.
abstract: OBJECTIVE
  Paraplegia due to ischemia-reperfusion (I/R) injury of the spinal cord is a devastating complication of thoracoabdominal aortic surgery. Cysteinyl leukotrienes are potent mediators of inflammation that are associated with I/R injury. The present study was designed to investigate the role of montelukast, a selective reversible CysLT1 receptor antagonist, on spinal cord I/R injury in an experimental model.
  
  
  METHODS
  Twenty-one male Sprague-Dawley rats were randomly assigned to three groups (n=7 per group) as G1 (no aortic occlusion and montelukast administration), G2 (45 min. aortic occlusion; no montelukast administration) and G3 (45 min. aortic occlusion, 10 mg/kg montelukast administration). After neurologic evaluation using the Motor Deficit Index (MDI) score at the 48th hour of reperfusion, lumbar spinal cords were removed for histopathological evaluation and immunohistochemical staining for HSP70, interleukin-6 and myeloperoxidase (MPO).
  
  
  RESULTS
  All rats in the G1 group had a normal neurological status and their MDI score was 0 (p < 0.05). The MDI score of G3 was significantly lower than G2 group (2.8 vs. 5.5; p < 0.05). Vacuolar congestion was found to be significantly lower in G1 than the other groups (p=0.0001). The interleukin-6 receptor level was found to be significantly lower in G3 group than the control group (p=0.013). There was no statistically significant difference found among the groups in terms of the degree of HSP70 and MPO staining.
  
  
  CONCLUSIONS
  Increased generation of leukotrienes in postischemic organs play an important role in I/R injury. The findings of the current study demonstrated that montelukast improved motor recovery and decreased IL-6 levels in spinal cord I/R injury.
authors.affiliation: Ankara Numune Education and Research Hospital, Department of Cardiovascular Surgery, Ankara, Turkey.
authors.forename: Kemal
authors.initials: K
authors.lastname: Korkmaz
authors.forename: Hikmet Selcuk
authors.initials: HS
authors.lastname: Gedik
authors.forename: Ali Baran
authors.initials: AB
authors.lastname: Budak
authors.forename: Ali Umit
authors.initials: AU
authors.lastname: Yener
authors.forename: Ertuğrul
authors.initials: E
authors.lastname: Kaya
authors.forename: Serhat Bahadır
authors.initials: SB
authors.lastname: Genc
authors.forename: Kerim
authors.initials: K
authors.lastname: Cagli
mesh_terms: D000085:Acetates / Q000494:pharmacology*; D000818:Animals; D003521:Cyclopropanes; D015850:Interleukin-6 / Q000096:biosynthesis; D020024:Leukotriene Antagonists / Q000494:pharmacology*; D008297:Male; D018696:Neuroprotective Agents / Q000494:pharmacology*; D010264:Paraplegia / Q000209:etiology; D009195:Peroxidase / Q000096:biosynthesis; D011804:Quinolines / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018077:Receptors, Leukotriene / Q000096:biosynthesis; D015427:Reperfusion Injury / Q000150:complications / Q000473:pathology*; D020760:Spinal Cord Ischemia / Q000150:complications / Q000473:pathology*; D013440:Sulfides
chemical_list: D000085:Acetates; D003521:Cyclopropanes; D015850:Interleukin-6; D020024:Leukotriene Antagonists; D018696:Neuroprotective Agents; D011804:Quinolines; D018077:Receptors, Leukotriene; D013440:Sulfides; D009195:Peroxidase; C083169:leukotriene D4 receptor; C093875:montelukast