title: An evaluation of white matter injury after spinal cord ischemia in rats: a comparison with gray matter injury.
abstract: We quantitatively assessed both gray and white matter injury after spinal cord ischemia in rats, and the relationship between the magnitude of gray and white matter injury was determined. Twenty-five male rats were anesthetized with isoflurane, and spinal cord ischemia (SCI) was induced by balloon intraaortic occlusion combined with hypotension. The animals were randomly allocated to one of the following three groups: animals with SCI for 12 min (SCI-12; n = 8), 15 min (SCI-15; n = 9), or those with sham operation (n = 8). Twenty-four hours after reperfusion, hindlimb motor function was assessed using the Basso-Beattie-Bresnahan scale scoring. Gray matter damage was assessed on the basis of the number of normal neurons in the ventral horn. White matter damage was assessed on the basis of the extent of vacuolation and amyloid precursor protein immunoreactivity in the ventral and ventrolateral white matter. There were significantly less normal neurons in the SCI-15 group compared with those in the SCI-12 and sham groups (P < 0.05). There was a significant positive correlation between the Basso-Beattie-Bresnahan scores and the number of normal neurons. The percentages of vacuolation areas in the SCI-15 group were significantly larger compared with those in the SCI-12 and sham groups (30% +/- 10% versus 9% +/- 7%, 0% +/- 0%, P < 0.05). Immunohistochemical analysis revealed increased amyloid precursor protein immunoreactivity in the swollen axons, especially in the SCI-15 group. There was a significant negative correlation between the number of normal neurons and percentages of vacuolation areas. These results indicate that both gray and white matter were injured after SCI in rats and the degree of white mater injury was correlated with the severity of gray matter injury after a relatively short recovery period.
authors.affiliation: Departments of Anesthesiology and 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: Toshinori
authors.initials: T
authors.lastname: Horiuchi
authors.forename: Satoki
authors.initials: S
authors.lastname: Inoue
authors.forename: Takanori
authors.initials: T
authors.lastname: Sakamoto
authors.forename: Mitsutoshi
authors.initials: M
authors.lastname: Nakamura
authors.forename: Noboru
authors.initials: N
authors.lastname: Konishi
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Furuya
mesh_terms: D016564:Amyloid beta-Protein Precursor / Q000032:analysis; D000818:Animals; D001794:Blood Pressure; D001812:Blood-Brain Barrier; D001921:Brain / Q000473:pathology*; D007150:Immunohistochemistry; D007511:Ischemia / Q000473:pathology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000098:blood supply*
chemical_list: D016564:Amyloid beta-Protein Precursor
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