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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
1996-11-27
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pubmed:abstractText |
Hyperkalemic cardioplegic solutions produce cardiac arrest during open heart surgery by depolarizing the sarcolemma. A recognized adverse effect of hyperkalemic cardioplegia is the possible development of ventricular dysfunction believed to be related to intracellular Ca2+ loading, a consequence of K(+)-induced membrane depolarization. Adenosine has been proposed as an adjunct to hyperkalemic cardioplegic solutions. However, it is not known whether adenosine can affect K(+)-induced membrane depolarization, and associated intracellular Ca2+ loading. Perforated patch-clamp method, applied to isolated single guinea-pig ventricular myocytes, revealed that adenosine (1 mM) did not significantly reduce the magnitude of K(+)-induced membrane depolarization (35.7 +/- 1.7 v 31.0 +/- 1.1 mV in the absence v presence of adenosine). Yet, adenosine significantly slowed the rate of K(+)-induced membrane depolarization (167 +/- 32.8 v 67.9 +/- 12.9 mV/min in the absence v presence of adenosine) without directly affecting Ca2+, Na+, and K+ currents. Imposed ramp-pulses, with different rates (ranging from 0.33 to 0.05 V/s), but same magnitude of depolarization (100 mV), demonstrated that reduction in the rate of membrane depolarization decreases net inward Ca2+ current. Indeed, in Fluo-3 loaded ventricular myocytes, imaged by laser confocal microscopy, adenosine (1 mM) prevented K(+)-induced intracellular Ca2+ loading. The present findings indicate that adenosine slows the rate of K(+)-induced membrane depolarization, and reduces K(+)-induced intracellular Ca2+ loading in ventricular myocytes. Such findings support the notion that adenosine may play a cardioprotective role in hyperkalemic cardioplegia.
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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,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Glyburide,
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 |
Jun
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pubmed:issn |
0022-2828
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
28
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1193-202
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8782061-Adenosine,
pubmed-meshheading:8782061-Animals,
pubmed-meshheading:8782061-Calcium Channels,
pubmed-meshheading:8782061-Cells, Cultured,
pubmed-meshheading:8782061-Glyburide,
pubmed-meshheading:8782061-Guinea Pigs,
pubmed-meshheading:8782061-Heart,
pubmed-meshheading:8782061-Heart Arrest, Induced,
pubmed-meshheading:8782061-Heart Ventricles,
pubmed-meshheading:8782061-Hyperkalemia,
pubmed-meshheading:8782061-Membrane Potentials,
pubmed-meshheading:8782061-Patch-Clamp Techniques,
pubmed-meshheading:8782061-Potassium,
pubmed-meshheading:8782061-Potassium Channels,
pubmed-meshheading:8782061-Time Factors,
pubmed-meshheading:8782061-Ventricular Function, Left
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pubmed:year |
1996
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pubmed:articleTitle |
Adenosine slows the rate of K(+)-induced membrane depolarization in ventricular cardiomyocytes: possible implication in hyperkalemic cardioplegia.
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pubmed:affiliation |
Departments of Medicine and Pharmacology, Mayo Clinic, Rochester, MN, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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