Document Detail

Noninvasive delayed limb ischemic preconditioning attenuates myocardial ischemia-reperfusion injury in rats by a mitochondrial K(ATP) channel-dependent mechanism.
MedLine Citation:
PMID:  21114361     Owner:  NLM     Status:  MEDLINE    
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.
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:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-11-29
Journal Detail:
Title:  Physiological research / Academia Scientiarum Bohemoslovaca     Volume:  60     ISSN:  1802-9973     ISO Abbreviation:  Physiol Res     Publication Date:  2011  
Date Detail:
Created Date:  2011-05-10     Completed Date:  2011-09-09     Revised Date:  2011-10-21    
Medline Journal Info:
Nlm Unique ID:  9112413     Medline TA:  Physiol Res     Country:  Czech Republic    
Other Details:
Languages:  eng     Pagination:  271-9     Citation Subset:  IM    
Department of Pharmacology, Tianjin Medical University, Tianjin, China.
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MeSH Terms
Arrhythmias, Cardiac / drug therapy,  prevention & control
Decanoic Acids / pharmacology
Glutathione Peroxidase / biosynthesis
Hydroxy Acids / pharmacology
Ischemic Preconditioning / methods*
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, Wistar
Superoxide Dismutase / biosynthesis
Xanthine Oxidase / biosynthesis
Reg. No./Substance:
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 Peroxidase; EC Dismutase; EC Oxidase

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