徳島大学 教育・研究者情報データベース(EDB)

1. 木下 倫子([徳島大学.病院.診療科.脳·神経·精神科.麻酔科])

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2. (英) Tsutsumi M. Yasuo

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3. (英) Fukuta Kohei

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4. (英) Kasai Asuka

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5. 田中 克哉([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.外科系.麻酔・疼痛治療医学]/[徳島大学.病院.診療科.脳·神経·精神科])

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(英) Isoflurane-induced postconditioning via mitochondrial calcium-activated potassium channels.

(英) Activation of the mitochondrial calcium-activated potassium (mKCa) channel reportedly confers resistance to myocardial ischemic stress. However, the role of the mKCa channel in postconditioning induced by volatile anesthetic remains unclear. Male Japanese white rabbits underwent coronary artery occlusion for 30 min followed by reperfusion for 3 h. Volatile anesthetic, isoflurane, was administered at 3 min prior to reperfusion for 5 min. Rabbits were injected with the mKCa channel blocker, iberiotoxin, or the mKCa channel opener, NS1619, at 8 min prior to reperfusion. Myocardial infarct size and the area at risk (AAR) were measured at the end of the experiment. Isoflurane significantly reduced infarct size (23.0 ± 9.8% of the AAR, P<0.05) compared with the control (44.0 ± 9.1%). Iberiotoxin abolished the cardioprotective impact of isoflurane (43.0 ± 11.6%), while iberiotoxin alone exerted no effect on infarct size (45.0 ± 9.5%). NS1619 and isoflurane/NS1619 both significantly reduced infarct size (21.0 ± 10.3% and 19.0 ± 8.8%, respectively, P<0.05 vs control group), but isoflurane/NS1619 showed no additional benefits compared with isoflurane alone. These results indicate that activation of the mKCa channel contribute isoflurane-induced postconditioning.

1. (英) Article.ELocationID: 10.2152/jmi.63.80

2. (英) Article.PublicationTypeList.PublicationType: Journal Article

3. (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't