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Cardioprotection by volatile anesthetics. Vascul Pharmacol 2005;42(5-6):243-52

Date

06/01/2005

Pubmed ID

15922257

DOI

10.1016/j.vph.2005.02.005

Scopus ID

2-s2.0-19444371408 (requires institutional sign-in at Scopus site)   57 Citations

Abstract

Preconditioning describes a very powerful endogenous mechanism by which the heart may be protected against ischemia and reperfusion injury. Transient administration of a volatile anesthetic before a prolonged ischemic episode reduces myocardial infarct size to a degree comparable to that observed during ischemic preconditioning. Many components of the signal transduction pathways responsible for cardioprotection are shared by anesthetic and ischemic preconditioning. Exposure to volatile anesthetics generates small "triggering" quantities of reactive oxygen species (ROS) by directly interacting with the mitochondrial electron transport chain or indirectly through a signaling cascade in which G-protein-coupled receptors, protein kinases, and mitochondrial ATP-sensitive potassium (K(ATP)) channels play important roles. Several clinical studies also suggest that preconditioning by volatile anesthetics exerts beneficial effects in patients undergoing cardiac surgery. This review summarizes some of the recent major developments in the understanding of cardioprotection by volatile anesthetics.

Author List

Bienengraeber MW, Weihrauch D, Kersten JR, Pagel PS, Warltier DC

Author

Dorothee Weihrauch DVM, PhD Research Scientist II in the Anesthesiology department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Anesthetics, Inhalation
Animals
Cardiotonic Agents
Humans
Ischemic Preconditioning, Myocardial