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The Evolution of Chemokine Release Supports a Bimodal Mechanism of Spinal Cord Ischemia and Reperfusion Injury
Author(s) -
Phillip D. Smith,
Ferenc Puskás,
Xianzhong Meng,
JoonHyung Lee,
Joseph C. Cleveland,
Michael J. Weyant,
David A. Fullerton,
T. Brett Reece
Publication year - 2012
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.111.080275
Subject(s) - medicine , mechanism (biology) , ischemia , spinal cord injury , chemokine , reperfusion injury , spinal cord , anesthesia , neuroscience , inflammation , cardiology , immunology , psychiatry , philosophy , epistemology , biology
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.

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