Source:http://linkedlifedata.com/resource/pubmed/id/15572051
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2004-12-1
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pubmed:abstractText |
Brief periods of ischemia that precede sustained ischemia can markedly reduce infarct size (IS), a phenomenon that is known as ischemic preconditioning (IP). Several investigators have shown that elevation of the intracellular Ca(2+) level ([Ca(2+)](i)) during the antecedent brief periods of ischemia triggers the cardioprotective mechanism of IP. Since opening of Ca(2+) activated K(+) (K(Ca)) channels is reported to be cardioprotective, we hypothesized that these channels may be involved in the cardioprotective mechanism of IP. In anesthetized open-chest dogs, myocardial ischemia/reperfusion injury was created by occlusion of the left anterior descending coronary artery (LAD) for 90 min followed by 6 h of reperfusion. First, we showed that the treatment with NS1619, a K(Ca) channel opener, reduced IS (IS in NS1619 group and control group, 19.8 +/- 5.5% vs. 45.4 +/- 3.5% of the area at risk, P < 0.05). Next, four cycles coronary occlusion for 5 min and reperfusion (IP) were performed before the 90-min occlusion with or without the infusion of potent K(Ca) channel inhibitors, iberiotoxin (IbTX) and charybdotoxin (ChTX). IP markedly reduced IS (IS in the IP group was 8.2 +/- 1.8%, P < 0.01 vs. control group). Infusion of either of K(Ca) channel blockers during IP blunted the IS-limiting effect of IP (IS in the IP + IbTX and IP + ChTX groups was 30.7 +/- 7.0% and 35.5 +/- 3.7%, respectively, P < 0.05, vs. IP group). However, the cardioprotective effect of IP was not blunted by the treatment with ChTX when treated only during reperfusion (14.0 +/- 4.1%). Thus, we conclude that the opening of K(Ca) channel is involved in early trigger phase of the molecular mechanism of IP.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0022-2828
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pubmed:author |
pubmed-author:AsanoYoshihiroY,
pubmed-author:AsanumaHiroshiH,
pubmed-author:FujitaMasashiM,
pubmed-author:FukushimaTomiT,
pubmed-author:HirataAkioA,
pubmed-author:HoriMasatsuguM,
pubmed-author:KimJiyoongJ,
pubmed-author:KitakazeMasafumiM,
pubmed-author:LiaoYulinY,
pubmed-author:NagamachiYokoY,
pubmed-author:NodeKoichiK,
pubmed-author:OkudaHirokoH,
pubmed-author:SanadaShojiS,
pubmed-author:ShinozakiYoshiroY,
pubmed-author:ShintaniYasunoriY,
pubmed-author:TakashimaSeijiS,
pubmed-author:TomoikeHitonobuH
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pubmed:issnType |
Print
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pubmed:volume |
37
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1213-8
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:15572051-Animals,
pubmed-meshheading:15572051-Calcium,
pubmed-meshheading:15572051-Dogs,
pubmed-meshheading:15572051-Ischemic Preconditioning, Myocardial,
pubmed-meshheading:15572051-Myocardial Infarction,
pubmed-meshheading:15572051-Myocardium,
pubmed-meshheading:15572051-Potassium Channels, Calcium-Activated
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pubmed:year |
2004
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pubmed:articleTitle |
Opening of Ca2+-activated K+ channels is involved in ischemic preconditioning in canine hearts.
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pubmed:affiliation |
Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Suita, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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