Source:http://linkedlifedata.com/resource/pubmed/id/15772780
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2005-3-17
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| pubmed:abstractText |
Left ventricular (LV) dilatation following myocardial infarction (MI) is a major determinant of the patient's prognosis, and myocardial energy metabolism may play a key role in LV remodeling. We aimed to investigate the relative timing of LV dilatation to LV function, myocardial energy regulation by uncoupling protein (UCP)-2, and cellular damage in the noninfarct zone. Myocardial infarction was produced in Sprague-Dawley rats by ligation of the coronary artery. The LV end-diastolic dimension (mm) increased (8.9+/-0.3 vs 6.8+/-0.8 in sham-operated rats, P<0.01) in association with elevation of the LV end-diastolic pressure (mmHg) (18+/-5 vs 6+/-2 in sham-operated rats) at 1 week following the ligation. At 4 weeks, the UCP-2 expression (180% of that in sham-operated rats) and LV end-diastolic dimension increased further (11.1+/-0.5, P<0.01) but there was no change in the LV end-diastolic pressure. The mechanisms for LV dilatation were quite different between the early and late stages after MI. In the late stage, augmentation of UCP-2 expression in the noninfarct zone may be related to the LV dilatation. Further examinations regarding the possibility of the protective role of UCP-2 are needed.
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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/Ion Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Mitochondrial Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species,
http://linkedlifedata.com/resource/pubmed/chemical/mitochondrial uncoupling protein 2
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| pubmed:status |
MEDLINE
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| pubmed:month |
Mar
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| pubmed:issn |
1615-2573
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
20
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
61-5
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| pubmed:meshHeading |
pubmed-meshheading:15772780-Animals,
pubmed-meshheading:15772780-Blotting, Northern,
pubmed-meshheading:15772780-Disease Models, Animal,
pubmed-meshheading:15772780-Echocardiography,
pubmed-meshheading:15772780-Hemodynamics,
pubmed-meshheading:15772780-Ion Channels,
pubmed-meshheading:15772780-Male,
pubmed-meshheading:15772780-Mitochondria, Heart,
pubmed-meshheading:15772780-Mitochondrial Proteins,
pubmed-meshheading:15772780-Myocardial Infarction,
pubmed-meshheading:15772780-Myocardium,
pubmed-meshheading:15772780-Oxidative Stress,
pubmed-meshheading:15772780-RNA, Messenger,
pubmed-meshheading:15772780-Rats,
pubmed-meshheading:15772780-Rats, Sprague-Dawley,
pubmed-meshheading:15772780-Reactive Oxygen Species,
pubmed-meshheading:15772780-Time Factors,
pubmed-meshheading:15772780-Up-Regulation,
pubmed-meshheading:15772780-Ventricular Dysfunction, Left,
pubmed-meshheading:15772780-Ventricular Remodeling
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| pubmed:year |
2005
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| pubmed:articleTitle |
Association of uncoupling protein-2 expression with increased reactive oxygen species in residual myocardium of the enlarged left ventricle after myocardial infarction.
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| pubmed:affiliation |
Second Department of Internal Medicine, School of Medicine, Kagawa University, Kagawa, Japan.
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| pubmed:publicationType |
Journal Article
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