Source:http://linkedlifedata.com/resource/pubmed/id/16775509
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2006-6-15
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pubmed:abstractText |
The structural left ventricular (LV) remodeling and contractile dysfunction of hearts with postinfarction LV remodeling are benefited by angiotensin II type 1 receptor (AT1) blocker. However, the myocardial bioenergetic consequences of AT1 blocker in these hearts are not known. To investigate, we used a porcine model of postinfarction LV remodeling produced by ligation of the left circumflex coronary artery. After infarction, 7 pigs received olmesartan medoxomil (2 mg/kg) for comparison against 9 untreated and 10 normal pigs. Measurements of hemodynamics, myocardial perfusion, and myocardial bioenergetics were taken 7 weeks postinfarction. The treated group had an LV-to-body weight ratio significantly lower than the untreated group (2.69 +/- 0.70, 2.96 +/- 0.51, 3.66 +/- 0.60 g/kg for control, treated, and untreated groups, respectively). The untreated group had a mean aortic pressure significantly higher than the control (73 +/- 16, 86 +/- 14, and 94 +/- 20 mm Hg, respectively). The subendocardial phosphocreatine-to-ATP ratios of the treated group were significantly higher than that of the untreated group. The untreated group, but not the treated group, had significant reductions in mitochondrial F0F1-ATPase subunits compared with controls. Congestive heart failure as evidenced by significant ascites (100 to 2000 mL) developed in 4 of the 9 untreated animals, but was absent in the treated group. Animals with heart failure demonstrated reductions in both mitochondrial F0F1-ATPase expression and myocardial high-energy phosphate levels. Thus, severe LV dysfunction and accompanying abnormal myocardial bioenergetic phenotype were prevented by the AT1 antagonist olmesartan medoxomil.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II Type 1 Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Imidazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphates,
http://linkedlifedata.com/resource/pubmed/chemical/Proton-Translocating ATPases,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrazoles,
http://linkedlifedata.com/resource/pubmed/chemical/olmesartan medoxomil
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0160-2446
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pubmed:author |
pubmed-author:AbdulMansoorM,
pubmed-author:GongGuangrongG,
pubmed-author:HuQingsongQ,
pubmed-author:IshibashiYukadaY,
pubmed-author:LeeJosephJ,
pubmed-author:LiuJingboJ,
pubmed-author:MurakamiYoY,
pubmed-author:OchiaiKoichiK,
pubmed-author:ShimadaToshioT,
pubmed-author:WangXiaohongX,
pubmed-author:ZhangJianyiJ
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pubmed:issnType |
Print
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pubmed:volume |
47
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
686-94
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:16775509-Angiotensin II Type 1 Receptor Blockers,
pubmed-meshheading:16775509-Animals,
pubmed-meshheading:16775509-Coronary Vessels,
pubmed-meshheading:16775509-Energy Metabolism,
pubmed-meshheading:16775509-Heart,
pubmed-meshheading:16775509-Heart Failure,
pubmed-meshheading:16775509-Imidazoles,
pubmed-meshheading:16775509-Magnetic Resonance Spectroscopy,
pubmed-meshheading:16775509-Mitochondria,
pubmed-meshheading:16775509-Myocardial Infarction,
pubmed-meshheading:16775509-Oxygen Consumption,
pubmed-meshheading:16775509-Phosphates,
pubmed-meshheading:16775509-Proton-Translocating ATPases,
pubmed-meshheading:16775509-Renin-Angiotensin System,
pubmed-meshheading:16775509-Swine,
pubmed-meshheading:16775509-Tetrazoles,
pubmed-meshheading:16775509-Ventricular Remodeling
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pubmed:year |
2006
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pubmed:articleTitle |
Functional and bioenergetic consequences of AT1 antagonist olmesartan medoxomil in hearts with postinfarction LV remodeling.
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pubmed:affiliation |
Department of Medicine, University of Minnesota Health Sciences, Minneapolis, MN 55455, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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