Document Detail


The myocardial contractile response to physiological stress improves with high saturated fat feeding in heart failure.
MedLine Citation:
PMID:  20511406     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Impaired myocardial contractile function is a hallmark of heart failure (HF), which may present under resting conditions and/or during physiological stress. Previous studies have reported that high fat feeding in mild to moderate HF/left ventricular (LV) dysfunction is associated with improved contractile function at baseline. The goal of this study was to determine whether myocardial function is compromised in response to physiological stress and to evaluate the global gene expression profile of rats fed high dietary fat after infarction. Male Wistar rats underwent ligation or sham surgery and were fed normal chow (NC; 10% kcal fat; Sham + NC and HF + NC groups) or high-fat chow (SAT; 60% kcal saturated fat; Sham + SAT and HF + SAT groups) for 8 wk. Myocardial contractile function was assessed using a Millar pressure-volume conductance catheter at baseline and during inferior vena caval occlusions and dobutamine stress. Steady-state indexes of systolic function, LV +dP/dt(max), stroke work, and maximal power were increased in the HF + SAT group versus the HF + NC group and reduced in the HF + NC group versus the Sham + NC group. Preload recruitable measures of contractility were decreased in HF + NC group but not in the HF + SAT group. beta-Adrenergic responsiveness [change in LV +dP/dt(max) and change in cardiac output with dobutamine (0-10 microg x kg(-1) x min(-1))] was reduced in HF, but high fat feeding did not further impact the contractile reserve in HF. The contractile reserve was reduced by the high-fat diet in the Sham + SAT group. Microarray gene expression analysis revealed that the majority of significantly altered pathways identified contained multiple gene targets correspond to cell signaling pathways and energy metabolism. These findings suggest that high saturated fat improves myocardial function at rest and during physiological stress in infarcted hearts but may negatively impact the contractile reserve under nonpathological conditions. Furthermore, high fat feeding-induced alterations in gene expression related to energy metabolism and specific signaling pathways revealed promising targets through which high saturated fat potentially mediates cardioprotection in mild to moderate HF/LV dysfunction.
Authors:
Jessica M Berthiaume; Molly S Bray; Tracy A McElfresh; Xiaoqin Chen; Salman Azam; Martin E Young; Brian D Hoit; Margaret P Chandler
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-05-28
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  299     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-30     Completed Date:  2010-08-30     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H410-21     Citation Subset:  IM    
Affiliation:
Dept. of Physiology and Biophysics, School of Medicine E521, Case Western Reserve Univ., 10900 Euclid Ave., Cleveland, OH 44106-4970, USA.
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MeSH Terms
Descriptor/Qualifier:
Adrenergic beta-Agonists / pharmacology
Animals
Cardiac Output
Dietary Fats / administration & dosage*,  blood
Disease Models, Animal
Dobutamine / pharmacology
Energy Metabolism
Fatty Acids / administration & dosage*,  blood
Gene Expression Profiling / methods
Gene Expression Regulation
Heart Failure / genetics,  metabolism,  physiopathology*,  ultrasonography
Male
Myocardial Contraction* / drug effects,  genetics
Myocardial Infarction / genetics,  metabolism,  physiopathology*,  ultrasonography
Oligonucleotide Array Sequence Analysis
Rats
Rats, Wistar
Recovery of Function
Signal Transduction
Stress, Physiological
Ventricular Dysfunction, Left / genetics,  physiopathology*,  ultrasonography
Ventricular Function, Left* / drug effects,  genetics
Ventricular Pressure
Grant Support
ID/Acronym/Agency:
HL-081857/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Adrenergic beta-Agonists; 0/Dietary Fats; 0/Fatty Acids; 34368-04-2/Dobutamine
Comments/Corrections

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