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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2006-12-22
pubmed:abstractText
We investigated the role of prostacyclin (PGI(2)) in the development of compression trauma-induced spinal cord injury (SCI) in rats. When measured after induction of SCI, tissue levels of 6-keto-PGF(1), a stable PGI(2) metabolite, thromboxane B(2) (TXB(2)), a stable metabolite of thromboxane A(2), myeloperoxidase (MPO) activity, and tumor necrosis factor (TNF) in the injured spinal cord segment were significantly increased, peaking at 2, 3, and 4 h after induction of SCI, respectively. Subcutaneous administration of indomethacin (IM), a non-selective cyclooxygenase (COX) inhibitor, completely inhibited increases in tissue levels of 6-keto-PGF(1) and TXB(2), while administration of NS-398, a selective inhibitor of COX-2, did not affect these increases. Although pretreatment with IM enhanced increases in tissue levels of MPO, TNF, and TNF mRNA and exacerbated both motor disturbances and histological damage in the spinal cord of animals subjected to SCI, pretreatment with NS-398 had no effect on any of these findings. Both iloprost, a stable analog of PGI(2), and leukocyte depletion significantly reversed changes in various variables and exacerbation of motor disturbances induced by IM pretreatment in animals subjected to SCI. These observations strongly suggested that compression trauma-induced increase in PGI(2) production in spinal cord tissue might be mainly mediated by COX-1 and PGI(2) might play a critical role in reduction of motor disturbances following SCI by inhibiting neutrophil accumulation through inhibition of TNF production.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0897-7151
pubmed:author
pubmed:issnType
Print
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1739-49
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Role of prostacyclin in the development of compression trauma-induced spinal cord injury in rats.
pubmed:affiliation
Department of Biodefense Medicine, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Japan.
pubmed:publicationType
Journal Article