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Anesthetic-induced myocardial protection in cardiac surgery: relevant mechanisms and clinical translation

DC FieldValueLanguage
dc.contributor.author소사라-
dc.contributor.author송종욱-
dc.contributor.author심재광-
dc.contributor.author최낙철-
dc.date.accessioned2019-12-18T00:20:09Z-
dc.date.available2019-12-18T00:20:09Z-
dc.date.issued2018-
dc.identifier.issn1975-5171-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/173003-
dc.description.abstractCardiac 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.-
dc.description.statementOfResponsibilityopen-
dc.languageKorean-
dc.publisherKorean Society of Anesthesiologists-
dc.relation.isPartOfAnesthesia and Pain Medicine-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleAnesthetic-induced myocardial protection in cardiac surgery: relevant mechanisms and clinical translation-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Anesthesiology and Pain Medicine (마취통증의학교실)-
dc.contributor.googleauthorSarah Soh-
dc.contributor.googleauthorJong Wook Song-
dc.contributor.googleauthorNakcheol Choi-
dc.contributor.googleauthorJae-Kwang Shim-
dc.identifier.doi10.17085/apm.2018.13.1.1-
dc.contributor.localIdA01960-
dc.contributor.localIdA02060-
dc.contributor.localIdA02060-
dc.contributor.localIdA02205-
dc.contributor.localIdA02205-
dc.contributor.localIdA05521-
dc.contributor.localIdA05521-
dc.relation.journalcodeJ00145-
dc.identifier.eissn2383-7977-
dc.subject.keywordAnalgesics-
dc.subject.keywordopioid-
dc.subject.keywordAnesthetics-
dc.subject.keywordinhalation-
dc.subject.keywordMyocardial ischemia-
dc.subject.keywordPropofol-
dc.subject.keywordReperfusion injury-
dc.contributor.alternativeNameSoh, Sa Rah-
dc.contributor.affiliatedAuthor소사라-
dc.contributor.affiliatedAuthor송종욱-
dc.contributor.affiliatedAuthor송종욱-
dc.contributor.affiliatedAuthor심재광-
dc.contributor.affiliatedAuthor심재광-
dc.contributor.affiliatedAuthor최낙철-
dc.contributor.affiliatedAuthor최낙철-
dc.citation.volume13-
dc.citation.number1-
dc.citation.startPage1-
dc.citation.endPage9-
dc.identifier.bibliographicCitationAnesthesia and Pain Medicine, Vol.13(1) : 1-9, 2018-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Anesthesiology and Pain Medicine (마취통증의학교실) > 1. Journal Papers

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