Myocardial High Energy Phosphate Stores in Cardiac Hypertrophy and Heart Failure

The aim of this study was to determine whether the impairment of contractility in the myocardium obtained from hypertrophied and failing hearts is due to a decreased store of energy and whether an imbalance exists between energy production and energy utilization in these hearts in vivo. Right ventri...

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Bibliographic Details
Published in:Circulation research 1967-09, Vol.21 (3), p.365-374
Main Authors: Pool, Peter E, Spann, James F, Buccino, Robert A, Sonnenblick, Edmund H, Braunwald, Eugene
Format: Article
Language:English
Subjects:
Adenosine Triphosphate - analysis
Animals
Cardiomyopathies - etiology
Cats
Heart Ventricles
Hypertrophy
In Vitro Techniques
Muscles - metabolism
Papillary Muscles - metabolism
Phosphocreatine - analysis
Pulmonary Artery
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Summary:The aim of this study was to determine whether the impairment of contractility in the myocardium obtained from hypertrophied and failing hearts is due to a decreased store of energy and whether an imbalance exists between energy production and energy utilization in these hearts in vivo. Right ventricular hypertrophy and right ventricular failure were produced in cats by constriction of the main pulmonary artery. Concentrations of creatine phosphate (CP) and adenosine triphosphate (ATP) were determined in samples removed from the right ventricles of these animals during life and in papillary muscles isolated from these same hearts. The papillary muscles from the cats with hypertrophy and failure exhibited depressed intrinsic contractility. The stores of ATP were normal in both the ventricular muscles and the papillary muscles in animals with hypertrophy and failure. Although the stores of CP were significantly depressed in the right ventricles of these animals, the stores had increased toward normal in papillary muscles isolated from these same hearts in vitro. The finding of normal energy stores in the papillary muscles from animals with hypertrophy and failure indicates that their intrinsically depressed contractility cannot be due to reductions of their energy stores in vivo such as were found in the samples from the ventricular wall. The differences between high energy phosphate stores in failing heart in vivo and these stores as they are replenished in vitro also indicate that the in vivo depressions are secondary to an imbalance between energy production and energy utilization in the overloaded, hypertrophied and failing heart.
ISSN:0009-7330
1524-4571
DOI:10.1161/01.res.21.3.365