• Feng Xiao.
• Department of Emergency Medicine, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA. fxiao@lsuhsc.edu
• Acad Emerg Med. 2002 Sep 1;9(9):933-46.

AbstractSudden cardiac arrest (CA) claims approximately 1,200 lives daily in the United States. Cardiopulmonary resuscitation attempts have so far achieved suboptimal results, and even when restoration of spontaneous circulation (ROSC) is achieved, about 30% of survivors suffer permanent brain damage. This illustrates the need for an improved basic scientific understanding of the pathophysiology of global cerebral injury caused by whole-body ischemia/reperfusion (I/R) injury following CA. Brain edema has been recently documented in experimental CA followed by one hour of ROSC. Brain edema has also been documented in CA and stroke patients by computed tomography or magnetic resonance imaging scanning, and has been shown to predict a poor neurologic outcome. The mechanisms underlying brain edema formation elicited by CA are unclear. New scientific findings of the roles of blood-brain barrier (BBB) permeability, matrix metalloproteinases (MMPs) of a family of proteases, aquaporin 4 (AQP4) of a family of membrane water-channel proteins, and the N-methyl-D-aspartate (NMDA) receptors in the mechanisms underlying CA-elicited brain edema were reviewed. By defining the roles of BBB permeability, MMPs, AQP4, and NMDA receptors in CA-induced brain edema formation, effective new therapeutic strategies to extend cellular and tissue survival, and preserve neurologic function following CA may be feasible.

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