title: Reevaluation of gray and white matter injury after spinal cord ischemia in rabbits.
abstract: BACKGROUND
  Although gray matter injury has been well characterized, the available data on white matter injury after spinal cord ischemia (SCI) in rabbits are limited. The current study was conducted to investigate the evolution of ischemia induced injury to gray and white matter and to correlate this damage to hind-limb motor function in rabbits subjected to SCI.
  
  
  METHODS
  Thirty-eight rabbits were randomly assigned to 24-h, 4-day, or 14-day reperfusion groups or a sham group (n = 9 or 10 per group). SCI was induced by occlusion of the infrarenal aorta for 16 min. Hind-limb motor function was assessed using the Tarlov scale (0 = paraplegia, 4 = normal). The gray matter damage was assessed on the basis of the number of normal neurons in the anterior spinal cord. White matter damage was assessed on the basis of the extent of vacuolation and accumulation of amyloid precursor protein immunoreactivity.
  
  
  RESULTS
  Tarlov scores gradually decreased and reached a nadir 14 days after reperfusion. There were no significant differences in the number of normal neurons among the 24-h, 4-day, and 14-day groups. The extent of vacuolation, expressed as a percent of total white matter area, was significantly greater in the 4-day and 14-day groups in comparison with the sham group. By contrast, there was no difference in vacuolation between the sham and 24-h groups. Amyloid precursor protein immunoreactivity was greater in the 4-day and 14-day groups.
  
  
  CONCLUSIONS
  The results in the current study show that SCI induced white matter injury as well as gray matter injury in a rabbit model of SCI. The time course for 14 days after reperfusion may differ among the gray and white matter damages and hind-limb motor function in rabbits subjected to SCI.
authors.affiliation: Department of Pathology, Nara Medical University, Kashihara, Nara, Japan.
authors.forename: Naoko
authors.initials: N
authors.lastname: Kurita
authors.forename: Masahiko
authors.initials: M
authors.lastname: Kawaguchi
authors.forename: Meiko
authors.initials: M
authors.lastname: Kakimoto
authors.forename: Yuri
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: Satoki
authors.initials: S
authors.lastname: Inoue
authors.forename: Mitsutoshi
authors.initials: M
authors.lastname: Nakamura
authors.forename: Noboru
authors.initials: N
authors.lastname: Konishi
authors.forename: Piyush M
authors.initials: PM
authors.lastname: Patel
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Furuya
mesh_terms: D016564:Amyloid beta-Protein Precursor / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000473:pathology*; D002452:Cell Count; D003627:Data Interpretation, Statistical; D006439:Hemodynamics / Q000502:physiology; D006614:Hindlimb / Q000502:physiology; D008297:Male; D009119:Muscle Contraction / Q000502:physiology; D018482:Muscle, Skeletal / Q000502:physiology; D009460:Neurologic Examination; D011817:Rabbits; D015427:Reperfusion Injury / Q000503:physiopathology; D020760:Spinal Cord Ischemia / Q000473:pathology*
chemical_list: D016564:Amyloid beta-Protein Precursor