• Vascular pharmacology · Apr 2005

    Review

    Cardioprotection by volatile anesthetics.

    • Martin W Bienengraeber, Dorothee Weihrauch, Judy R Kersten, Paul S Pagel, and David C Warltier.
    • Department of Anesthesiology, Pharmacology and Toxicology, (Division of Cardiovascular Diseases), Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, Wisconsin 53226, USA. mbieneng@mcw.edu
    • Vascul. Pharmacol. 2005 Apr 1;42(5-6):243-52.

    AbstractPreconditioning 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.

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