• Phillip F Pratt, Chen Wang, Dorothee Weihrauch, Martin W Bienengraeber, Judy R Kersten, Paul S Pagel, and David C Warltier.
• Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
• Curr Opin Anaesthesiol. 2006 Aug 1; 19 (4): 397-403.

Purpose Of ReviewPharmacological interventions may play a prominent role in reducing organ damage in response to physiologic stress. A growing body of evidence indicates that volatile anesthetics exert protective effects against ischemia-reperfusion injury in vivo. Administration of volatile anesthetics before prolonged coronary artery occlusion and reperfusion has been shown to produce cardioprotection, a phenomenon termed anesthetic-induced preconditioning. Endogenous signal transduction proteins, reactive oxygen species, mitochondria, and ion channels have been implicated in anesthetic-induced preconditioning, and new data regarding the triggering and effector roles for these various components have been discovered that advance our understanding of the mechanisms responsible for anesthetic-induced preconditioning. This review will update and integrate these recent data into the current mechanistic model of anesthetic-induced preconditioning.Recent FindingsDespite a wealth of data from animal studies, the mechanism by which preconditioning with volatile anesthetics alleviates ischemic injury remains incompletely understood. Recent data have identified important interactions between reactive oxygen species and key intracellular signal transduction enzymes and proteins implicated in anesthetic-induced preconditioning.SummaryThis review highlights the major recent findings examining mechanisms of volatile anesthetic cardioprotection.

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