Preconditioning and postresuscitation injury.
A major challenge in improving cardiac arrest survival is organ injury that occurs after the return of spontaneous circulation. This postresuscitation injury may result in as many as 90% of such patients not surviving to hospital discharge. Preconditioning, an adaptive physiologic response found in multiple organs and species, may help protect against such injury of ischemic tissue when reperfused at the return of spontaneous circulation. A better understanding of how preconditioning may alter postresuscitation injury is important for two major reasons. First, it is one of the most protective adaptations currently known in nature that attenuates ischemia-reperfusion injury. Pharmacologic and nonpharmacologic means to quickly trigger and perhaps augment this response have the potential to greatly improve survival from the global ischemia of cardiac arrest. Second, potential targets of preconditioning-such as the adenosine triphosphate-sensitive potassium channel and NAD(P)H oxidases-likely play important roles in the postresuscitation phase of cardiac arrest, and their modification may be important components of future treatment for patients with return of spontaneous circulation. The evidence for postresuscitation injury at the cellular level and its modification by preconditioning are discussed.
Vanden Hoek
Terry L
TL
Section of Emergency Medicine, Department of Medicine, and the Emergency Resuscitation Center, University of Chicago, Chicago, IL 60637, USA. thoek@medicine.bsd.uchicago.edu
D002478:Cells, Cultured; D006801:Humans; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism; D009249:NADP / Q000378:metabolism; D017382:Reactive Oxygen Species
D017382:Reactive Oxygen Species; D009249:NADP