title: How many ligations of bilateral segmental arteries cause ischemic spinal cord dysfunction? An experimental study using a dog model.
abstract: METHODS
  Segmental arteries were interrupted bilaterally for up to 7 levels to study the effects on spinal cord blood flow and neurologic function in dogs.
  
  
  OBJECTIVE
  To examine how many ligations of bilateral segmental arteries cause ischemic spinal cord dysfunction.
  
  
  BACKGROUND
  Interruption of bilateral segmental arteries for up to 3 levels has been reported not to damage spinal cord function. However, to our knowledge, the effects of ligating more than 3 levels have not yet been clearly determined.
  
  
  METHODS
  There were 15 dogs divided into 5 groups: sham group, no ligation; group 1, ligation of bilateral segmental arteries at 3 levels (T11-T13); group 2, at 4 levels (T10-T13); group 3, at 5 levels (T10-L1); and group 4, at 7 levels (T9-L2). Spinal cord blood flow at T12 measured by laser Doppler flowmetry, and spinal cord-evoked and motor-evoked potentials were measured simultaneously until 10 hours after ligation. Neurologic function was assessed using a modified Tarlov grading system 1 week after operation in 20 other dogs divided into 4 groups (1, 2, 3, and 4).
  
  
  RESULTS
  Spinal cord blood flow was 99.3%, 80.7%, 71.5%, 44.3%, and 25.0% in the sham group, and groups 1, 2, 3, and 4, respectively, 10 hours after ligation. Abnormal spinal cord-evoked potentials were observed in 2 of 3 dogs in group 3 and all 3 in group 4. Abnormal motor-evoked potentials were observed in 1 of 3 dogs in group 3 and all 3 in group 4. Postoperative neurologic evaluation identified all 5 dogs in groups 1 and 2, respectively, and 3 in group 3 as having grade 5. There were 2 dogs in group 3 and 3 in group 4 that had grade 4, and 2 in group 4 had grade 3.
  
  
  CONCLUSIONS
  Interruption of bilateral segmental arteries at > or =5 consecutive levels risks producing a spinal cord ischemia capable of injuring the spinal cord.
authors.affiliation: Department of Orthopaedic Surgery, School of Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa, 920-8641, Japan. seikei@kenroku.kanazawa-u.ac.jp
authors.forename: Yoshiyasu
authors.initials: Y
authors.lastname: Fujimaki
authors.forename: Norio
authors.initials: N
authors.lastname: Kawahara
authors.forename: Katsuro
authors.initials: K
authors.lastname: Tomita
authors.forename: Hideki
authors.initials: H
authors.lastname: Murakami
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Ueda
mesh_terms: D000818:Animals; D001158:Arteries / Q000502:physiology; D004195:Disease Models, Animal; D004285:Dogs; D019054:Evoked Potentials, Motor / Q000502:physiology; D005260:Female; D008026:Ligation; D008159:Lumbar Vertebrae / Q000098:blood supply / Q000503:physiopathology; D012039:Regional Blood Flow / Q000502:physiology; D013116:Spinal Cord / Q000098:blood supply* / Q000503:physiopathology*; D020760:Spinal Cord Ischemia / Q000503:physiopathology*; D013904:Thoracic Vertebrae / Q000098:blood supply / Q000503:physiopathology