Source:http://linkedlifedata.com/resource/pubmed/id/10409190
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1 Pt 2
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pubmed:dateCreated |
1999-8-30
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pubmed:abstractText |
The adenosine agonist 2-chloro-N(6)-cyclopentyladenosine (CCPA) induces delayed ischemic protection in vivo. We hypothesized that this protection is mediated by opening of ATP-sensitive K(+) (K(ATP)) channels and increased synthesis of 72-kDa heat shock protein (HSP 72). Six groups (n = 9-13 animals/group) of animals were studied: group I, control rabbits that received no treatment; group II, animals given glibenclamide (0.3 mg/kg iv) 30 min before ischemia; group III, animals given 5-hydroxydecanoate (5-HD; 5 mg/kg iv) 15 min before ischemia; group IV, rabbits treated with CCPA (0.1 mg/kg iv) 24 h before ischemia; and groups V and VI, CCPA-treated animals that received the K(ATP)-channel blockers glibenclamide or 5-HD, respectively, 30 or 15 min before ischemia. All animals were subjected to ischemia by 30 min of coronary artery occlusion followed by 3 h of reperfusion. Risk area was delineated by injection of 10% Evans blue dye, and infarct size was determined by triphenyltetrazolium staining. Action potential duration (APD) was measured with an epicardial electrode. HSP 72 was measured by Western blotting. CCPA caused a significant reduction in infarct size [12.02 +/- 1.0 vs. 40.0 +/- 3.8% (%area at risk) in controls, P < 0.01] that was blocked by glibenclamide (36.2 +/- 3.1%, P < 0.01) and 5-HD (35.0 +/- 2.9%, P < 0.01). Glibenclamide and 5-HD did not change infarct size in control rabbits. These blockers significantly suppressed ischemia-induced APD shortening in control and CCPA-treated animals. CCPA treatment did not induce HSP 72 in hearts. These data suggest that adenosine-initiated delayed protection is mediated via opening of K(ATP) channels but does not involve the synthesis of HSP 72.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/2-chloro-N(6)cyclopentyladenosine,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Cardiovascular Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
277
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H128-35
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10409190-Action Potentials,
pubmed-meshheading:10409190-Adenosine,
pubmed-meshheading:10409190-Adenosine Triphosphate,
pubmed-meshheading:10409190-Animals,
pubmed-meshheading:10409190-Cardiovascular Agents,
pubmed-meshheading:10409190-Ischemic Preconditioning, Myocardial,
pubmed-meshheading:10409190-Male,
pubmed-meshheading:10409190-Myocardial Infarction,
pubmed-meshheading:10409190-Potassium Channels,
pubmed-meshheading:10409190-Rabbits,
pubmed-meshheading:10409190-Time Factors
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pubmed:year |
1999
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pubmed:articleTitle |
Delayed preconditioning with adenosine is mediated by opening of ATP-sensitive K(+) channels in rabbit heart.
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pubmed:affiliation |
Division of Cardiology, Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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