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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
1996-11-21
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pubmed:abstractText |
With 2 microM methylisobutyl amiloride (MIA), an inhibitor of Na+/H+ exchange, we tested the hypothesis that ion imbalance due to H+/Na+/Ca2+ exchange exacerbates reperfusion injury and arrhythmias. Isolated rat hearts were subjected to 25-min global ischemia and 30-min reperfusion. In the MIA-treated group, MIA was added throughout the perfusion protocol. Left ventricular pressure (LVP), arrhythmias, myocardial Na+ and K+ content, 45Ca2+ uptake, and the levels of energy metabolites were analyzed. The recovery of LV developed pressure (LVDP) and +dP/dt and -dP/dt were improved in the MIA group (53 vs. 80, 71 vs. 86, 77 vs. 94%: each p < 0.05). MIA inhibited the increase in Na+ content and the decrease in K+ content that occurred at the end of the ischemic phase and reduced 45Ca2+ uptake after reperfusion (28.6 vs. 17.1, 248 vs. 296, 2.79 vs. 1.36 microM/g dry weight of tissue; each p < 0.05). The incidence of ventricular tachycardia (VT) or ventricular fibrillation (VF) was lower in the MIA group [VT 11 of 20 (55%) vs. 4 of 20 (20%), p < 0.05; VF 13 of 20, (65%) vs. 6 of 20 (30%), 0.05 < p < 0.1], although the incidence of VF just escaped statistical significance. ATP level was higher in the MIA group after the ischemic phase and reperfusion (5.3 vs. 9.9, 12.3 vs. 14.7 microM/g dry weight of tissue; each p < 0.05). Our results suggest that MIA reduced reperfusion arrhythmias and improved functional recovery in isolated rat hearts subjected to global ischemia apparently by preserving high-energy phosphates during ischemia and by inhibiting Na+/H+ exchange, with attenuated cellular imbalance between Na+ and Ca2+.
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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/5-(N-methyl-N-isobutyl)amiloride,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Amiloride,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Hydrogen Antiporter
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0160-2446
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
27
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
794-801
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:8761845-Adenosine Triphosphate,
pubmed-meshheading:8761845-Amiloride,
pubmed-meshheading:8761845-Animals,
pubmed-meshheading:8761845-Calcium,
pubmed-meshheading:8761845-Heart,
pubmed-meshheading:8761845-Hemodynamics,
pubmed-meshheading:8761845-Male,
pubmed-meshheading:8761845-Myocardial Contraction,
pubmed-meshheading:8761845-Myocardial Reperfusion Injury,
pubmed-meshheading:8761845-Myocardium,
pubmed-meshheading:8761845-Rats,
pubmed-meshheading:8761845-Rats, Sprague-Dawley,
pubmed-meshheading:8761845-Sodium,
pubmed-meshheading:8761845-Sodium-Hydrogen Antiporter,
pubmed-meshheading:8761845-Ventricular Function, Left
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pubmed:year |
1996
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pubmed:articleTitle |
Effect of methylisobutyl amiloride on [Na+]i, reperfusion arrhythmias, and function in ischemic rat hearts.
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pubmed:affiliation |
Department of Geriatric Medicine, Keio University School of Medicine, Tokyo, Japan.
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pubmed:publicationType |
Journal Article,
Comparative Study,
In Vitro
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