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Cardiovascular Research 1996 31(1):163-171; doi:10.1016/S0008-6363(95)00183-2
© 1996 by European Society of Cardiology
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Copyright © 1996, European Society of Cardiology

Energy metabolism patterns in mammalian myocardium adapted to chronic physiopathological conditions

André Rossi and Sylviane Lortet1

Laboratoire de Physiologie Cellulaire Cardiaque, Université Joseph Fourier, BP 53 X-38041, Grenoble CEDEX, France

Objective: When the myocardium is subjected to a chronic overload, it enlarges and a major restructuring of all organelles and cellular functions occurs. The changes occurring at the level of the contractile apparatus are well documented; less is known about the alterations in the energy status of the hypertrophied cardiomyocyte. The purpose of this paper is firstly to provide a brief review of the data published on this topic and secondly to analyse previously published data drawn from studies devoted to the evaluation of the capacity of the ATP-producing processes to respond to an acute change in workload. Methods: Several different chronic conditions were studied in rats: senescence, hypertension, chronic hypoxia, and administration of thyroid hormone. The pattern of the metabolic response of the heart to acute changes in workload was characterized by alterations in the concentrations of phosphocreatine, inorganic phosphate and ATP followed in isolated heart by 31P-NMR spectroscopy. Results: In most of the models studied the pattern of these changes was very similar to that observed in controls. The only exceptions concerned the hearts of young hypertensive rats and those of animals subjected to a cumulated overload (hypertension + thyroid hormone). Conclusion: Our results demonstrate that the regulation of energy metabolism was well preserved in spite of the extensive restructuring that occurs in rat hearts subjected to different chronic conditions which could affect the energy balance of the cardiomyocyte.

KEYWORDS Energy metabolism; Heart; Overload; Hypertrophy; Phosphorylated compounds

1 The experimental results cited in the paper have been obtained in collaboration with: J. Aussedat, S. Grably, N. Lavanchy, V. Novel, A. Ray, Laboratoire de Physiologie Cellulaire Cardiaque, Grenoble, France; H.-G. Zimmer, M. Heckmann, Department of Physiology of the Univesity of Munich, Germany; J. Sassard, M. Vincent, Laboratoire d'Etudes Expérimentales de l'Hypertension, Lyon, France; C. Caldarera, C. Guamieri, C. Finelli, Departimento di Biochimica, Università di Bologna, Bologna, Italy.


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