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Anesthetic-induced myocardial protection in cardiac surgery: relevant mechanisms and clinical translation
Anesth Pain Med 2018;13(1):1-9
Published online January 31, 2018
© 2018 Korean Society of Anesthesiologists.

Sarah Soh1,2, Jong Wook Song1,2, Nakcheol Choi1, and Jae-Kwang Shim1,2
1Department of Anesthesiology and Pain Medicine, 2Anesthesia and Pain Research Institute, Yonsei University College of Medicine, Seoul, Korea
Correspondence to: Jae-Kwang Shim, M.D., Ph.D.
Department of Anesthesiology and Pain Medicine, Anesthesia and Pain Research Institute, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, Korea
Tel: 82-2-2228-8515
Fax: 82-2-364-2951
E-mail: aneshim@yuhs.ac
ORCID
http://orcid.org/0000-0001-9093-9692
Received October 24, 2017; Accepted December 6, 2017.
cc This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Cardiac surgery is still associated with complications such as adverse perioperative cardiovascular events. Over the past two decades, many studies have shown that volatile anesthetics and opioids provide myocardial protection against ischemia-reperfusion injury in a similar manner as ischemic conditioning. First (1–2 hours) and second (24–72 hours) windows of protection are provided, the underlying mechanisms for which involve activation of G-protein-coupled receptors, protein kinases, and the opening of adenosine triphosphate-sensitive potassium channels. These processes ultimately result in inhibition of the mitochondrial permeability transition pore. Post-conditioning can also be effective when treatment is applied in the proximity of reperfusion. Although propofol lacks these conditioning effects, it acts as a strong antioxidant and protects the myocardium by attenuating oxidative stress related to reperfusion injury. Clinical evidence favors the use of volatile anesthetics over propofol in terms of reduced cardiac enzyme release, length of hospital stay, and mortality. However, the existing evidence level is insufficient to draw a definite conclusion regarding the mortality benefit of one anesthetic over the others. In addition, many common clinical conditions, such as advanced age, hyperglycemia/diabetes, and hypertrophy, have been shown to mitigate the protective efficacy of the anesthetics, although this effect also lacks clinical validation. Propofol may also abolish the protective effects of volatile anesthetics and opioids by scavenging reactive oxygen species, an essential trigger for pre-conditioning. The following review addresses these issues from a clinical perspective.
Key Words : Analgesics, opioid, Anesthetics, inhalation, Myocardial ischemia, Propofol, Reperfusion injury.


January 2018, 13 (1)
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