| Noninvasive delayed limb ischemic preconditioning attenuates myocardial ischemia-reperfusion injury in rats by a mitochondrial K(ATP) channel-dependent mechanism. | |
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MedLine Citation:
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PMID: 21114361 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We previously demonstrated in rats that noninvasive delayed limb ischemic preconditioning (LIPC) induced by three cycles of 5-min occlusion and 5-min reperfusion of the left hind limb per day for three days confers the same cardioprotective effect as local ischemic preconditioning of the heart, but the mechanism has not been studied in depth. The aim of this project was to test the hypothesis that delayed LIPC enhances myocardial antioxidative ability during ischemia-reperfusion by a mitochondrial K(ATP) channel (mito K(ATP))-dependent mechanism. Rats were randomized to five groups: ischemia-reperfusion (IR)-control group, myocardial ischemic preconditioning (MIPC) group, LIPC group, IR-5HD group and LIPC-5HD group. The MIPC group underwent local ischemic preconditioning induced by three cycles of 5-min occlusion and 5-min reperfusion of the left anterior descending coronary arteries. The LIPC and LIPC-5HD groups underwent LIPC induced by three cycles of 5-min occlusion and 5-min reperfusion of the left hind limb using a modified blood pressure aerocyst per day for three days. All rats were subjected to myocardial ischemia-reperfusion injury. The IR-5HD and LIPC-5HD groups received the mito K(ATP) channel blocker 5-hydroxydecanoate Na (5-HD) before and during the myocardial ischemia-reperfusion injury. Compared with the IR-control group, both the LIPC and MIPC groups showed an amelioration of ventricular arrhythmia, reduced myocardial infarct size, increased activities of total superoxide dismutase, manganese-superoxide dismutase (Mn-SOD) and glutathione peroxidase, increased expression of Mn-SOD mRNA and decreased xanthine oxidase activity and malondialdehyde concentration. These beneficial effects of LIPC were prevented by 5-HD. In conclusion, delayed LIPC offers similar cardioprotection as local IPC. These results support the hypothesis that the activation of mito K(ATP) channels enhances myocardial antioxidative ability during ischemia-reperfusion, thereby contributing, at least in part, to the anti-arrhythmic and anti-infarct effects of delayed LIPC. |
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Authors:
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Y-N Wu; H Yu; X-H Zhu; H-J Yuan; Y Kang; J-J Jiao; W-Z Gao; Y-X Liu; J-S Lou |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-11-29 |
Journal Detail:
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Title: Physiological research / Academia Scientiarum Bohemoslovaca Volume: 60 ISSN: 1802-9973 ISO Abbreviation: Physiol Res Publication Date: 2011 |
Date Detail:
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Created Date: 2011-05-10 Completed Date: 2011-09-09 Revised Date: 2011-10-21 |
Medline Journal Info:
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Nlm Unique ID: 9112413 Medline TA: Physiol Res Country: Czech Republic |
Other Details:
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Languages: eng Pagination: 271-9 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, Tianjin Medical University, Tianjin, China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arrhythmias, Cardiac / drug therapy, prevention & control Decanoic Acids / pharmacology Glutathione Peroxidase / biosynthesis Hydroxy Acids / pharmacology Ischemic Preconditioning / methods* Male Malondialdehyde / metabolism Myocardial Infarction / drug therapy, prevention & control Myocardial Reperfusion Injury / drug therapy, prevention & control* Myocardium / chemistry, metabolism Potassium Channel Blockers / pharmacology Potassium Channels / drug effects, metabolism* Rats Rats, Wistar Superoxide Dismutase / biosynthesis Xanthine Oxidase / biosynthesis |
| Chemical | |
Reg. No./Substance:
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0/Decanoic Acids; 0/Hydroxy Acids; 0/Potassium Channel Blockers; 0/Potassium Channels; 0/mitochondrial K(ATP) channel; 542-78-9/Malondialdehyde; 624-00-0/5-hydroxydecanoic acid; EC 1.11.1.9/Glutathione Peroxidase; EC 1.15.1.1/Superoxide Dismutase; EC 1.17.3.2/Xanthine Oxidase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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