Ischemia reperfusion injury [Neurosurgery Wiki]

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====== Ischemia reperfusion injury ======

see [[Cerebral ischemia-reperfusion injury]].

sse [[Spinal cord ischemia reperfusion injury]].

Previous studies have shown that  Ischemia [[reperfusion injury]] (IRI) contributes to the injury process in the central nervous system (CNS), through the activation of the [[immune system]]
((Gökce EC, et al. Neuroprotective effects of [[thymoquinone]] against spinal cord ischemia-reperfusion injury by attenuation of inflammation, oxidative stress, and apoptosis. J Neurosurg Spine. 2016;24(6):949–959. doi: 10.3171/2015.10.SPINE15612.))
((Dimitrijevic OB, Stamatovic SM, Keep RF, Andjelkovic AV. Absence of the chemokine receptor CCR2 protects against cerebral ischemia/reperfusion injury in mice. Stroke. 2007;38(4):1345–1353. doi: 10.1161/01.STR.0000259709.16654.8f.))
((Chen Y, et al. Overexpression of monocyte chemoattractant protein 1 in the brain exacerbates ischemic brain injury and is associated with recruitment of inflammatory cells. J Cereb Blood Flow Metab. 2003;23(6):748–755.))
((Smith PD, et al. The evolution of chemokine release supports a bimodal mechanism of spinal cord ischemia and reperfusion injury. Circulation. 2012;126(11 Suppl 1):S110–S117.))
((Strecker JK, Minnerup J, Gess B, Ringelstein EB, Schäbitz WR, Schilling M. Monocyte chemoattractant protein-1-deficiency impairs the expression of IL-6, IL-1β and G-CSF after transient focal ischemia in mice. PLoS One. 2011;6(10):e25863 doi: 10.1371/journal.pone.0025863.)).