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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6 Pt 2
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pubmed:dateCreated |
1992-1-23
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pubmed:abstractText |
We examined influences of a blocker (glibenclamide) and an opener (nicorandil) of the ATP-sensitive potassium (KATP) channel on extracellular K concentration [( K+]e), as well as the myocardial function and metabolites during global ischemia and reperfusion in Langendorff-perfused rat heart preparation. In control hearts, [K+]e began to rise 20 s after the onset of ischemia up to an initial peak (8.3 +/- 0.3 mM) at 2.5 +/- 0.7 min, then fell to 6.0 +/- 0.8 mM after 8.2 +/- 0.7 min, and then rose progressively to 14.6 +/- 0.8 mM at the end of 30 min of ischemia. Glibenclamide (50 microM) reduced the initial peak of [K+]e to 7.2 +/- 0.3 mM (P less than 0.01), and nicorandil (200 microM) increased it to 9.4 +/- 0.6 mM (P less than 0.01). There were no significant differences in [K+]e values among all groups at the end of ischemia. During ischemia, nicorandil decreased the time to mechanical arrest from 1.9 +/- 0.1 min to 1.5 +/- 0.1 min, whereas it was increased by glibenclamide to 2.7 +/- 0.4 min. In control hearts, the time to onset of ischemic contracture was 14.7 +/- 1.8 min. Nicorandil delayed onset of contracture and glibenclamide accelerated it. Thus we have confirmed that some part of the early increase in [K+]e during ischemia is attributable to K+ efflux through the KATP channel in our model, and opening of the KATP channel may contribute to a rapid reduction of the contractility of the ischemic myocardium that subsequently protects the myocardium against further ischemic injury.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Glyburide,
http://linkedlifedata.com/resource/pubmed/chemical/Niacinamide,
http://linkedlifedata.com/resource/pubmed/chemical/Nicorandil,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
261
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H1864-71
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:1836311-Adenosine Triphosphate,
pubmed-meshheading:1836311-Animals,
pubmed-meshheading:1836311-Coronary Disease,
pubmed-meshheading:1836311-Glyburide,
pubmed-meshheading:1836311-Heart,
pubmed-meshheading:1836311-Kinetics,
pubmed-meshheading:1836311-Male,
pubmed-meshheading:1836311-Myocardial Contraction,
pubmed-meshheading:1836311-Myocardial Reperfusion,
pubmed-meshheading:1836311-Niacinamide,
pubmed-meshheading:1836311-Nicorandil,
pubmed-meshheading:1836311-Potassium,
pubmed-meshheading:1836311-Potassium Channels,
pubmed-meshheading:1836311-Rats,
pubmed-meshheading:1836311-Rats, Inbred Strains,
pubmed-meshheading:1836311-Ventricular Function, Left
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pubmed:year |
1991
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pubmed:articleTitle |
Effects of glibenclamide and nicorandil on cardiac function during ischemia and reperfusion in isolated perfused rat hearts.
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pubmed:affiliation |
Division of Cardiovascular Surgery, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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