Cardioprotection by volatile anesthetics: new applications for old drugs?
OBJECTIVE
Pharmacological 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.


RESULTS
Despite 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.


CONCLUSIONS
This review highlights the major recent findings examining mechanisms of volatile anesthetic cardioprotection.
Pratt
Phillip F
PF
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
Wang
Chen
C
Weihrauch
Dorothee
D
Bienengraeber
Martin W
MW
Kersten
Judy R
JR
Pagel
Paul S
PS
Warltier
David C
DC
D018685:Anesthetics, Inhalation / Q000494:pharmacology / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects; D002316:Cardiotonic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D006331:Heart Diseases / Q000517:prevention & control*; D006801:Humans; D054086:KATP Channels; D008928:Mitochondria / Q000187:drug effects; D010539:Permeability; D024661:Potassium Channels, Inwardly Rectifying / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects
D018685:Anesthetics, Inhalation; D002316:Cardiotonic Agents; D054086:KATP Channels; D024661:Potassium Channels, Inwardly Rectifying; D017382:Reactive Oxygen Species; C092520:uK-ATP-1 potassium channel