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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1995-10-5
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pubmed:abstractText |
Cardiac dysfunctions such as myocardial functional failure and ventricular arrhythmia have been largely attributed to intracellular Ca2+ overload. One of the mechanisms of intracellular Ca2+ overload involves a rapid influx of Ca2+ via Na(+)-Ca2+ exchange during the reperfusion which utilizes the accumulation of Na+ in myocytes during ischemic cardiac arrest. Possible sources of the intracellular Na+ accumulation include Na+ channel, Na(+)-H+ exchange, Na(+)-Ca2+ exchange, and Na+ background current. In this study, we studied the role of the Na+ background current in intracellular Na+ accumulation during the cardiac arrest by measuring the Na+ background current in guinea pig ventricular myocytes with whole cell clamp method and evaluating the effects of cardioprotective drugs on the Na+ background current. The results were as follows: (1) The Na+ background inward current at -40 mV membrane potential was larger at Ca2+ free solution than 1.8 mM Ca2+ solution. (2) The Na+ background current was not affected by verapamil. (3) 2 microM O-(N, N-hexamethylene)-amiloride (HMA) decreased the Na+ background current at negative membrane potential. (4) The new cardioprotective drug, R 56865, decreased the Na+ background current. These results suggest that the Na+ background current plays a role in increasing the intracellular Na+ activity during high K+ cardioplegia and the blocking effect of myoprotective drugs, such as R 56865, on the Na+ background current may contribute to myocardial protection after 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/Amiloride,
http://linkedlifedata.com/resource/pubmed/chemical/Benzothiazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Piperidines,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium,
http://linkedlifedata.com/resource/pubmed/chemical/R 56865,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/Thiazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Verapamil
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0513-5796
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
36
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
278-86
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:7660679-Amiloride,
pubmed-meshheading:7660679-Animals,
pubmed-meshheading:7660679-Benzothiazoles,
pubmed-meshheading:7660679-Guinea Pigs,
pubmed-meshheading:7660679-Heart,
pubmed-meshheading:7660679-Heart Arrest, Induced,
pubmed-meshheading:7660679-Myocardium,
pubmed-meshheading:7660679-Piperidines,
pubmed-meshheading:7660679-Potassium,
pubmed-meshheading:7660679-Sodium,
pubmed-meshheading:7660679-Thiazoles,
pubmed-meshheading:7660679-Verapamil
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pubmed:year |
1995
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pubmed:articleTitle |
Cardioprotective drugs decrease the Na+ background current.
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pubmed:affiliation |
Department of Physiology, Inha University College of Medicine, Inchon, Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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