title: Effects of vascular endothelial growth factor on ischemic spinal cord injury caused by aortic cross-clamping in rabbits.
abstract: BACKGROUND
  Spinal cord injury remains a devastating complication of thoracic and thoracoabdominal aortic operations. We aim to investigate neuro-protective role of vascular endothelial growth factor (VEGF) administered to rabbits after occlusion against ischemia-reperfusion (I/R) injury.
  
  
  METHODS
  Occlusion of the abdominal aorta was applied to adult rabbits, followed by removal of aortic clamp and reperfusion. The abdominal aortas of New Zealand White albino rabbits were occluded for 30 min. Experimental groups were as follows: control group (sham operation group, n = 7), I/R group (n = 9) undergoing occlusion but receiving no pharmacologic intervention, and VEGF-treated group (n = 7) receiving 0.8 microg/kg VEGF intravenously after occlusion. Neurological status was assessed at 6, 24, and 48 h after the operation. All animals were killed at 48 h after the operation. Spinal cords were harvested for histopathologic and biochemical analyses.
  
  
  RESULTS
  According to Tarlov's scale, neurological status of the rabbits at postoperative h 48 was better in the VEGF-treated group compared to the I/R group (P < 0.05). Decreased tissue and serum malondialdehyde levels and increased tissue and serum glutathione levels were observed in VEGF-treated group (P < 0.05). In the same group tissue and serum nitrate levels were decreased (P < 0.05). Histopathologic analyses demonstrated typical morphological changes characteristic of necrosis in the I/R group. VEGF attenuated ischemia-induced necrosis.
  
  
  CONCLUSIONS
  This is the first study that shows the effects of VEGF administered after occlusion on induced oxidative damage to injured spinal cords. VEGF administration may significantly reduce the incidence of spinal cord injury following temporary aortic occlusion.
authors.affiliation: Department of Physiology, Faculty of Medicine, Gazi University, Ankara, Turkey. oze@gazi.edu.tr
authors.forename: Eser
authors.initials: E
authors.lastname: Oz Oyar
authors.forename: Ozgür
authors.initials: O
authors.lastname: Kardeş
authors.forename: Ayhan
authors.initials: A
authors.lastname: Korkmaz
authors.forename: Suna
authors.initials: S
authors.lastname: Omeroğlu
mesh_terms: D000818:Animals; D001011:Aorta / Q000601:surgery*; D004195:Disease Models, Animal; D005978:Glutathione / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D011817:Rabbits; D015427:Reperfusion Injury / Q000517:prevention & control; D013116:Spinal Cord / Q000378:metabolism / Q000473:pathology; D013119:Spinal Cord Injuries / Q000209:etiology* / Q000378:metabolism / Q000517:prevention & control*; D020760:Spinal Cord Ischemia / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D013525:Surgical Instruments; D042461:Vascular Endothelial Growth Factor A / Q000494:pharmacology*
chemical_list: D042461:Vascular Endothelial Growth Factor A; D009569:Nitric Oxide; D008315:Malondialdehyde; D005978:Glutathione