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The evolution of chemokine release supports a bimodal mechanism of spinal cord ischemia and reperfusion injury.
MedLine Citation:
PMID:  22965970     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
BACKGROUND: Paraplegia remains a devastating complication of thoracic aortic surgery. The mechanism of the antecedent spinal cord ischemia and reperfusion injury (IR) remains poorly described. IR involves 2 injuries, an initial ischemic insult and subsequent inflammatory amplification of the injury. This mechanism is consistent with the clinical phenomenon of delayed onset paraplegia. This study sought to characterize the inflammatory response in the spinal cord after IR and hypothesized that this would support a bimodal mechanism of injury.
METHODS AND RESULTS: Male C57Bl/6 mice were subjected to 5 minutes of aortic arch and left subclavian occlusion with subsequent reperfusion to generate spinal cord ischemia. Functional outcomes were scored at 12-hour intervals. Spinal cords were harvested after 0, 6, 12, 18, 24, 36, and 48 hours of reperfusion. Cytokine levels were analyzed using a mouse magnetic bead-based multiplex immunoassay. Inflammatory chemokine concentrations (interleukin [IL]-1β, IL-6, keratinocyte-derived cytokine, macrophage inflammatory protein-1α, monocyte chemotactic protein-1, RANTES, and tumor necrosis factor-α) peaked at 6 hours and 36 to 48 hours after reperfusion. Functional scores reflected initial gain in function with subsequent decline, inversely proportional to cytokine levels. Immunofluorescent staining demonstrated microglia activation at 12 and 48 hours.
CONCLUSIONS: Spinal cord ischemia and reperfusion injury occurs in 2 phases, correlating to increases in inflammatory chemokines release and microglial activation. These observations chronologically parallel the too-common clinical syndrome of delayed-onset paraplegia. Understanding the molecular pathogenesis of this injury may allow future intervention to prevent this devastating complication.
Authors:
Phillip D Smith; Ferenc Puskas; Xianzhong Meng; Joon H Lee; Joseph C Cleveland; Michael J Weyant; David A Fullerton; T Brett Reece
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Circulation     Volume:  126     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-09-11     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  S110-7     Citation Subset:  AIM; IM    
Affiliation:
University of Colorado Anschutz Medical Campus, Mail Stop C310, Academic Office One, Room 6602, 12631 E 17 Ave, Aurora, CO 80045. brett.reece@ucdenver.edu.
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