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Year : 2018  |  Volume : 4  |  Issue : 1  |  Page : 1-13

Hypothermia and brain inflammation after cardiac arrest

1 Department of Medicine, Virginia Commonwealth University, Falls Church, Virginia; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA
2 Department of Pharmacy, Johns Hopkins University School of Medicine, Baltimore, MD, USA
3 Department of Neurology; Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA

Correspondence Address:
Dr. Romergryko G Geocadin
600 N Wolfe Street, Phipps 455, Baltimore, MD 21287
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/bc.BC_4_18

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The cessation (ischemia) and restoration (reperfusion) of cerebral blood flow after cardiac arrest (CA) induce inflammatory processes that can result in additional brain injury. Therapeutic hypothermia (TH) has been proven as a brain protective strategy after CA. In this article, the underlying pathophysiology of ischemia-reperfusion brain injury with emphasis on the role of inflammatory mechanisms is reviewed. Potential targets for immunomodulatory treatments and relevant effects of TH are also discussed. Further studies are needed to delineate the complex pathophysiology and interactions among different components of immune response after CA and identify appropriate targets for clinical investigations.

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