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Preconditioning of the myocardium by volatile anesthetics. Curr Med Chem Cardiovasc Hematol Agents 2004 Jul;2(3):249-55

Date

08/24/2004

Pubmed ID

15320790

DOI

10.2174/1568016043356318

Scopus ID

2-s2.0-3042701428 (requires institutional sign-in at Scopus site)   9 Citations

Abstract

Cardiovascular disease continues to be a major health problem. Tremendous efforts have been invested in clinical and laboratory research in the hopes of decreasing the risk of patients with cardiovascular disease undergoing cardiac and non-cardiac surgeries. A powerful endogenous mechanism of cardioprotection, termed ischemic preconditioning, was reported in a laboratory setting whereby the myocardium can be preconditioned by a brief ischemic episode and protected against a subsequent prolonged ischemic attack. Since this initial observation, several pharmacological agents have been demonstrated to mimic ischemic preconditioning. These include opioids, potassium channel openers such as pinacidil and diazoxide, and adenosine agonists. Recently, volatile anesthetics were found to be powerful cardiac preconditioning agents. Infarct size reduction as the result of anesthetic-induced preconditioning paralleled that of ischemic preconditioning. The use of volatile anesthetics as preconditioning agents in high-risk patients undergoing cardiac and non-cardiac surgeries can potentially result in the reduction of morbidity and disability in this class of patients. However, to fully realize the potential use of this novel property of volatile anesthetics, the underlying mechanism of anesthetic-induced preconditioning would need to be elucidated. This review highlights the major recent findings on the cardioprotective effects of volatile anesthetics.

Author List

Kwok WM, Aizawa K

Author

Wai-Meng Kwok PhD Professor in the Anesthesiology department at Medical College of Wisconsin




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

Anesthetics, Inhalation
Cardiovascular Agents
Humans
Ischemic Preconditioning, Myocardial
Myocardial Infarction
Potassium Channels
Signal Transduction