Abstract
BackgroundCanine intervertebral disc πherniation causes a naturally-occurring spinal cord injury (SCI) that bears critical similarities to human SCI with respect to both injury pathomechanisms and treatment. As such, it has tremendous potential to enhance our understanding of injury biology and the preclinical evaluation of novel therapies. Currently, there is limited understanding of the role of arachidonic acid metabolites in canine SCI.ResultsThe CSF concentrations of PLA2 and PGE2 were higher in SCI dogs compared to control dogs (p = 0.0370 and 0.0273, respectively), but CSF LCT4 concentration in SCI dogs was significantly lower than that in control dogs (p < 0.0001). Prostaglandin E2 concentration in the CSF was significantly and positively associated with increased severity of SCI at the time of sampling (p = 0.041) and recovery 42 days post-injury (p = 0.006), as measured by ordinal behavioral scores.ConclusionArachidonic acid metabolism is altered in dogs with SCI, and these data suggest that these AA metabolites reflect injury severity and recovery, paralleling data from other model systems.
Highlights
Canine intervertebral disc πherniation causes a naturally-occurring spinal cord injury (SCI) that bears critical similarities to human SCI with respect to both injury pathomechanisms and treatment
The cerebrospinal fluid (CSF) concentration of prostaglandin E2 (PGE2) was significantly higher in SCI dogs compared to control dogs, and significant relationships existed between CSF PGE2 concentration, initial SCI severity, as well as 42-day post-SCI recovery
This study suggests that lipoprotein associated lipoprotein-associated phospholipase A2 (PLA2), leukotriene C4 (LTC4), and PGE2 are all associated with SCI and may provide information relevant to recovery of function
Summary
Canine intervertebral disc πherniation causes a naturally-occurring spinal cord injury (SCI) that bears critical similarities to human SCI with respect to both injury pathomechanisms and treatment. Several experimental animal models of spinal cord injury (SCI) have been established, including contusion, laceration, clip compression, and crush in a variety of species [1,2,3]. Chronic dysregulation of 5-LOX and COX pathways following experimental spinal cord contusion results in depletion of lipid metabolites, altered amino acid biosynthesis, and pro-inflammatory events. Limited investigation of these pathways has occurred in large animal models of SCI. In one study that utilized an experimental canine model of compression/contusion, LTs and PGs were increased within the cerebrospinal fluid (CSF) 1 day following injury and remained elevated for approximately 7 days after the primary event [23]
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