Isoflurane-induced postconditioning via mitochondrial calcium-activated potassium channels
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- Kinoshita Michiko
- Department of Anesthesiology, Tokushima University Hospital
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- M. Tsutsumi Yasuo
- Department of Anesthesiology, Institute of Biomedical Sciences, Tokushima University Graduate School
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- Fukuta Kohei
- Department of Anesthesiology, Tokushima University Hospital
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- Kasai Asuka
- Department of Anesthesiology, Tokushima University Hospital
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- Tanaka Katsuya
- Department of Anesthesiology, Institute of Biomedical Sciences, Tokushima University Graduate School
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Purpose: 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. Methods: 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. Results: 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. Conclusion: These results indicate that activation of the mKCa channel contribute isoflurane-induced postconditioning. J. Med. Invest. 63: 80-84, February, 2016
収録刊行物
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- The Journal of Medical Investigation
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The Journal of Medical Investigation 63 (1.2), 80-84, 2016
国立大学法人 徳島大学医学部
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詳細情報 詳細情報について
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- CRID
- 1390282679222487680
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- NII論文ID
- 130005141048
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- NII書誌ID
- AA11166929
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- ISSN
- 13496867
- 13431420
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- PubMed
- 27040058
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- 本文言語コード
- en
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- データソース種別
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