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Decreased rates of substrate oxidation ex vivo predict the onset of heart failure and contractile dysfunction in rats with pressure overload

Cardiovascular research, 2010-06, Vol.86 (3), p.461-470 [Peer Reviewed Journal]

2015 INIST-CNRS ;ISSN: 0008-6363 ;EISSN: 1755-3245 ;DOI: 10.1093/cvr/cvp414 ;PMID: 20035032 ;CODEN: CVREAU

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Title:
Decreased rates of substrate oxidation ex vivo predict the onset of heart failure and contractile dysfunction in rats with pressure overload
Author: Doenst, Torsten ; Pytel, Gracjan ; Schrepper, Andrea ; Amorim, Paulo ; Färber, Gloria ; Shingu, Yasushige ; Mohr, Friedrich W. ; Schwarzer, Michael
Subjects: Animals ; Biological and medical sciences ; Blood Pressure ; Cardiology. Vascular system ; Cardiovascular system ; Cell Respiration ; Disease Models, Animal ; Echocardiography ; Energy Metabolism ; Fatty Acids - metabolism ; Glucose - metabolism ; Heart ; Heart failure ; Heart Failure - etiology ; Heart Failure - metabolism ; Heart Failure - physiopathology ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; Hypertension - complications ; Hypertension - metabolism ; Hypertrophy, Left Ventricular - etiology ; Hypertrophy, Left Ventricular - metabolism ; Hypertrophy, Left Ventricular - physiopathology ; Investigative techniques, diagnostic techniques (general aspects) ; Male ; Medical sciences ; Mitochondria, Heart - metabolism ; Myocardial Contraction ; Myocardium - metabolism ; Myocardium - pathology ; Oxidation-Reduction ; Pressure overload ; Pulmonary Edema - etiology ; Pulmonary Edema - metabolism ; Pulmonary Edema - physiopathology ; Rats ; Rats, Sprague-Dawley ; Stroke Volume ; Substrate oxidation predictive for diagnosis of heart failure ; Time Factors ; Ultrasonic investigative techniques ; Ventricular Dysfunction, Left - etiology ; Ventricular Dysfunction, Left - metabolism ; Ventricular Dysfunction, Left - physiopathology ; Ventricular Function, Left
Is Part Of: Cardiovascular research, 2010-06, Vol.86 (3), p.461-470
Description: Aims Left ventricular hypertrophy is a risk factor for heart failure. However, it also is a compensatory response to pressure overload, accommodating for increased workload. We tested whether the changes in energy substrate metabolism may be predictive for the development of contractile dysfunction. Methods and results Chronic pressure overload was induced in Sprague–Dawley rats by aortic arch constriction for 2, 6, 10, or 20 weeks. Contractile function in vivo was assessed by echocardiography and by invasive pressure measurement. Glucose and fatty acid oxidation as well as contractile function ex vivo were assessed in the isolated working heart, and respiratory capacity was measured in isolated cardiac mitochondria. Pressure overload caused progressive hypertrophy with normal ejection fraction (EF) at 2, 6, and 10 weeks, and hypertrophy with dilation and impaired EF at 20 weeks. The lung-to-body weight ratio, as marker for pulmonary congestion, was normal at 2 weeks (indicative of compensated hypertrophy) but significantly increased already after 6 and up to 20 weeks, suggesting the presence of heart failure with normal EF at 6 and 10 weeks and impaired EF at 20 weeks. Invasive pressure measurements showed evidence for contractile dysfunction already after 6 weeks and ex vivo cardiac power was reduced even at 2 weeks. Importantly, there was impairment in fatty acid oxidation beginning at 2 weeks, which was associated with a progressive decrease in glucose oxidation. In contrast, respiratory capacity of isolated mitochondria was normal until 10 weeks and decreased only in hearts with impaired EF. Conclusion Pressure overload-induced impairment in fatty acid oxidation precedes the onset of congestive heart failure but mitochondrial respiratory capacity is maintained until the EF decreases in vivo. These temporal relations suggest a tight link between impaired substrate oxidation capacity in the development of heart failure and contractile dysfunction and may imply therapeutic and prognostic value.
Publisher: Oxford: Oxford University Press
Language: English
Identifier: ISSN: 0008-6363
EISSN: 1755-3245
DOI: 10.1093/cvr/cvp414
PMID: 20035032
CODEN: CVREAU
Source: GFMER Free Medical Journals
MEDLINE
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Decreased rates of substrate oxidation ex vivo predict the onset of heart failure and contractile dysfunction in rats with pressure overload

2015 INIST-CNRS ;ISSN: 0008-6363 ;EISSN: 1755-3245 ;DOI: 10.1093/cvr/cvp414 ;PMID: 20035032 ;CODEN: CVREAU

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