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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
8
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pubmed:dateCreated |
2010-7-21
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pubmed:abstractText |
A high-lipid diet (HLD) may lead to adverse left ventricular (LV) remodeling and endothelial dysfunction in conditions of hemodynamic stress. Although congenital absence of nitric oxide synthase 3 (NOS3) leads to adverse LV remodeling after transverse aortic constriction (TAC), the effects of a HLD in this state remains unknown. Wild-type (WT) and NOS3 knockout mice (NOS3(-/-)) were randomized into the following 4 groups: 1) WT + low-lipid diet (LLD) (10% of energy); 2) WT + HLD (60% of energy); 3) NOS3(-/-) + LLD; and 4) NOS3(-/-) + HLD for a total of 12 wk. After 1 wk of randomization, TAC was performed on all groups. Serial echocardiography revealed a decrease in LV ejection fraction (LVEF) in WT and NOS3(-/-) mice fed the HLD compared with those fed the LLD diet at 12 wk post-TAC. Mice fed the NOS3(-/-) + HLD diet had a lower LVEF compared with mice in the other 3 groups (P < 0.05). There was greater myocyte hypertrophy, interstitial fibrosis, and percentage change in plasma cholesterol concentrations in the NOS3(-/-) + HLD group 12 wk post-TAC compared with the other 3 groups. Although high molecular weight fibroblast growth factor-2, a marker of cardiac hypertrophy, was more upregulated in the NOS3(-/-) + HLD group than in the other groups, markers of the renin-angiotensin system did not differ among them. A HLD potentiates LV dysfunction in NOS3(-/-) mice in a chronic pressure overload state.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1541-6100
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pubmed:author |
pubmed-author:AhmadieRoienR,
pubmed-author:AzordeganNazilaN,
pubmed-author:BageSheriS,
pubmed-author:DixonIan M CIM,
pubmed-author:FangTielanT,
pubmed-author:JassalDavinder SDS,
pubmed-author:KardamiElissavetE,
pubmed-author:LeKhuongK,
pubmed-author:LytwynMatthewM,
pubmed-author:MoghadasianMohammed HMH,
pubmed-author:RattanSunilS,
pubmed-author:SantiagoJon-JonJJ,
pubmed-author:WalkerJonathanJ,
pubmed-author:ZhaoZhaohuiZ
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pubmed:issnType |
Electronic
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pubmed:volume |
140
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1438-44
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pubmed:meshHeading |
pubmed-meshheading:20554900-Animals,
pubmed-meshheading:20554900-Aorta,
pubmed-meshheading:20554900-Blood Pressure,
pubmed-meshheading:20554900-Cholesterol,
pubmed-meshheading:20554900-Constriction,
pubmed-meshheading:20554900-Dietary Fats,
pubmed-meshheading:20554900-Echocardiography,
pubmed-meshheading:20554900-Energy Intake,
pubmed-meshheading:20554900-Fibroblast Growth Factor 2,
pubmed-meshheading:20554900-Heart Ventricles,
pubmed-meshheading:20554900-Hypertension,
pubmed-meshheading:20554900-Hypertrophy, Left Ventricular,
pubmed-meshheading:20554900-Male,
pubmed-meshheading:20554900-Mice,
pubmed-meshheading:20554900-Mice, Inbred C57BL,
pubmed-meshheading:20554900-Mice, Knockout,
pubmed-meshheading:20554900-Molecular Weight,
pubmed-meshheading:20554900-Muscle Cells,
pubmed-meshheading:20554900-Myocardium,
pubmed-meshheading:20554900-Nitric Oxide Synthase Type III,
pubmed-meshheading:20554900-Stroke Volume,
pubmed-meshheading:20554900-Ventricular Dysfunction, Left
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pubmed:year |
2010
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pubmed:articleTitle |
A high-lipid diet potentiates left ventricular dysfunction in nitric oxide synthase 3-deficient mice after chronic pressure overload.
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pubmed:affiliation |
Institute of Cardiovascular Sciences, St. Boniface General Hospital, University of Manitoba, Winnipeg, Manitoba, Canada.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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