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After opening the chest, all rats underwent 30-min coronary artery occlusion followed by 2-h reperfusion. The rats received low-dose (0.15 mg/kg) or high-dose (0.5 mg/kg) fasudil or diazoxide, an m-KATP channel opener, at 10 mg/kg, just before reperfusion under normoglycemic or hyperglycemic conditions. In another group, rats received 5-hydroxydecanoic acid (5HD), an m-KATP channel blocker, at 10 mg/kg, before high-dose fasudil. Myocardial infarct size was expressed as a percentage of area at risk (AAR).Results: Under normoglycemia, low-dose and high-dose fasudil and diazoxide reduced myocardial infarct size (23 ± 8%, 21 ± 9% and 21 ± 10% of AAR, respectively) compared with that in the control (42 ± 7%). Under hyperglycemia, low-dose fasudil (40 ± 11%) and diazoxide (44 ± 14%) could not exert this beneficial effect, but high-dose fasudil reduced myocardial infarct size in the same manner as under normoglycemia (21 ± 13%). 5HD prevented fasudil-induced reduction of myocardial infarct size (42 ± 13%).Conclusion: Fasudil induces PostC against myocardial infarction via activation of m-KATP channels in the rat. 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High-dose fasudil preserves postconditioning against myocardial infarction under hyperglycemia in rats: Role of mitochondrial KATP channels
http://hdl.handle.net/10069/29070
http://hdl.handle.net/10069/2907005c26b48-a52f-4ddb-a51d-32aa519a2532
名前 / ファイル | ライセンス | アクション |
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CarDia11_28.pdf (769.9 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2012-08-24 | |||||
タイトル | ||||||
タイトル | High-dose fasudil preserves postconditioning against myocardial infarction under hyperglycemia in rats: Role of mitochondrial KATP channels | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Fasudil | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Hyperglycemia | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Mitochondrial KATP channels | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Myocardial infarction | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Postconditioning | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Ichinomiya, Taiga
× Ichinomiya, Taiga× Cho, Sungsam× Higashijima, Ushio× Matsumoto, Shuhei× Maekawa, Takuji× Sumikawa, Koji |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Background: The current study was carried out to determine whether fasudil hydrochloride (fasudil), a Rho-kinase inhibitor, has myocardial postconditioning (PostC) activity under hyperglycemia as well as normoglycemia, and if so, whether the effects could be mediated by mitochondrial ATP-sensitive potassium (m-KATP) channels.Methods: Male Sprague-Dawley rats were anesthetized with sodium pentobarbital. After opening the chest, all rats underwent 30-min coronary artery occlusion followed by 2-h reperfusion. The rats received low-dose (0.15 mg/kg) or high-dose (0.5 mg/kg) fasudil or diazoxide, an m-KATP channel opener, at 10 mg/kg, just before reperfusion under normoglycemic or hyperglycemic conditions. In another group, rats received 5-hydroxydecanoic acid (5HD), an m-KATP channel blocker, at 10 mg/kg, before high-dose fasudil. Myocardial infarct size was expressed as a percentage of area at risk (AAR).Results: Under normoglycemia, low-dose and high-dose fasudil and diazoxide reduced myocardial infarct size (23 ± 8%, 21 ± 9% and 21 ± 10% of AAR, respectively) compared with that in the control (42 ± 7%). Under hyperglycemia, low-dose fasudil (40 ± 11%) and diazoxide (44 ± 14%) could not exert this beneficial effect, but high-dose fasudil reduced myocardial infarct size in the same manner as under normoglycemia (21 ± 13%). 5HD prevented fasudil-induced reduction of myocardial infarct size (42 ± 13%).Conclusion: Fasudil induces PostC against myocardial infarction via activation of m-KATP channels in the rat. Although hyperglycemia attenuates the PostC, high-dose fasudil can restore cardioprotection. | |||||
書誌情報 |
Cardiovascular Diabetology 巻 11, 号 28, p. 1-9, 発行日 2012-03-22 |
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出版者 | ||||||
出版者 | BioMed Central | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 14752840 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1186/1475-2840-11-28 | |||||
権利 | ||||||
権利情報 | © 2012 Ichinomiya et al; licensee BioMed Central Ltd. | |||||
権利 | ||||||
権利情報 | This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | Cardiovascular Diabetology, 11(28), pp.1-9; 2012 |