Respiratory Chain O2 Requirements and the Metabolic Answer to Diffuse Ischemia of Mechanically Overloaded Left Ventricular Myocardium

  • J. Moravec
  • J. Nzonzi
  • C. Bowe
  • D. Feuvray
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 169)


Cardiac adaptation to mechanical overload proceeds in a three step manner (Meerson, 1969). After a short transitional period, a new steady state is usually attained before the heart fails. This period of enhanced metabolic activity (compensatory cardiac hypertrophy) can sometimes last over several weeks. In rats with a surgically induced aorto-caval communication (Hatt et al., 1980a), the compensated cardiac hypertrophy can persist over several months. Morphologically, the hearts from rats with a prolongated volume overload exhibit a decreased vascularization of the left ventricle (Rakusan et al., 1980). At the cellular level, the persistence of an activation of protein synthesis was suggested (Hatt et al., 1980a), the size of the left ventricular myocytes are increasing (Hatt et al., 1980b) and quantitative changes in intracellular organization appear (Anversa et al., 1971). The most striking modification is the increase in numerical density of the mitochondria resulting in an improved surface/volume ratio of mitochondria and decreased oxygen requirements for mitochondrial function (decreased cytochrome oxidase apparent KM [O2]; Moravec et al., 1981). In this work we tried to quantify the range of intracellular Po2’s compatible with the unimpaired mitochondrial function (full oxidation of the cytochrome oxidase).


Chain Acyl Cytochrome Oxidase Pyridine Nucleotide Adenine Nucleotide Translocase Coronary Flow Rate 
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  1. Anversa, P., Vitali-Mazza, L., Visioli, O., and Marchetti, G., 1971, Experimental cardiac hypertrophy: a quantitative ultrastructure study, J. Mol. Cell. Cardiol., 3: 213.PubMedCrossRefGoogle Scholar
  2. Chance, B., 1976, Pyridine nucleotide as an indicator of the oxygen requirements for energy-linked functions of the mitochondria, Circ. Res., 38(Suppl. 1): 31.Google Scholar
  3. Chua, B., and Shrago, E., 1977, Reversible inhibition of adenine nucleotide translocase in bovine heart mitochondria by long chain acyl CoA esters. Comparison with atractyloside and bon-krekik acid, J. Biol. Chenu, 252: 6711.Google Scholar
  4. Feuvray, D., 1981, Structural, functional and metabolic correlates in ischemic hearts: effect of substrates, Am. J. Physiol., 240: 391.Google Scholar
  5. Garland, P.E., Shepherd, D., and Yates, D.W., 1965, Steady state concentrations of coenzyme A, acetyl coenzyme A and long chain fatty acyl CoA in rat liver mitochondria oxidizing palmitate, Biochem. J., 97: 587.PubMedGoogle Scholar
  6. Hatt, P.Y., Rakusan, K., Gastineau, P., Laplace, M., and Cluzeaud, F., 1980a, Aorto-caval fistula in rat: an experimental model of heart overloading, Bas. Res. Cardiol., 75: 105.CrossRefGoogle Scholar
  7. Hatt, P.Y., Rakusan, K., Gastineau, P., and Laplace, M., 1980b, Morphometry and ultrastructure of heart hypertrophy induced by chronic volume overload, J. Mol. Cell. Cardiol., 11: 989.CrossRefGoogle Scholar
  8. Hochachka, P.W., 1980, “Living Without Oxygen”, Harvard University Press, Cambridge, London.Google Scholar
  9. Jöbsis, F.F., 1977, What is molecular oxygen sensor: What is a transduction process, in.: “Tissue Hypoxia and Ischemia”, M. Reivich, R. Coburn, S. Lahiri, B. Chance, eds., Plenum Press, New York.Google Scholar
  10. Leniger-Follert, E., and Lübbers, D.W., 1973, Determination of local myoglobin concentration in the guinea pig heart, Pflügers Arch., 341: 271.PubMedCrossRefGoogle Scholar
  11. Lübbers, D.W., and Niesel, W., 1959, Der Kurzzeit-Spektralanalysator. Ein schnellarbeitendes Spektralphotometer zur laufenden Messung von Absorptions-bzw. Extinktionsspektren, Pflügers Arch. Ges. Physiol., 268: 286.CrossRefGoogle Scholar
  12. Mc Garry, J.D., and Foster, D.W., 1976, An improved and simplified radio isotope assay for the determination of free and esterified carnitine, J. Lipid Res., 17: 277.PubMedGoogle Scholar
  13. Meerson, F.Z., 1969, The myocardium in hyperfunction hypertrophy and failure, Cire, Res., 25(Suppl. 2): 1.Google Scholar
  14. Mela, L., Goodwin, C.W., and Miller, L.D., 1976, In vivo control of mitochondrial enzyme concentrations and activity by oxygen, Am. J. Physiol., 231: 1811.PubMedGoogle Scholar
  15. Moravec, J., 1980, Possible relationship between tissue levels of long chain acyl CoA and the ability of the overloaded myocardium to oxidize an excess of reduced pyridine nucleotide, FEBS Lett., 113: 134.PubMedCrossRefGoogle Scholar
  16. Moravec, J., Corsin, A., Owen, P., and Opie, L.H., 1974, Effect of increased aortic pressure on fluorescence emission of isolated rat heart, J. Mol. Cell. Cardiol., 6: 187.PubMedCrossRefGoogle Scholar
  17. Moravec, J., Moravec, M., and Hatt P.Y., 1981, Rate of pyridine nucleotide oxidation and cytochrome oxidase interaction with intracellular oxygen in hearts from rats with compensated volume overload, Pflügers Arch., 392: 106.PubMedCrossRefGoogle Scholar
  18. Neely, J.R., Garber, D., Mc Donough, K., and Idell-Wenger, J., 1979, Relationships between ventricular function and intermediates of fatty acid metabolic during myocardial ischemia, in: “Ischemic Myocardium and Antianginal Drugs”, M.M. Winsburg, ed., Plenum Press, New York.Google Scholar
  19. Neely, J.R., Rovetto, M.J., Whitmar, J.T., and Morgan, H.E., 1973, Effect of ischemia on ventricular function and metabolism in the isolated working rat hearts, Am. J. Physiol., 225: 651.PubMedGoogle Scholar
  20. Rakusan, K., Moravec, J., and Hatt, P.Y., 1980, Regional capillary supply to the normal and hypertrophied rat heart, Microvasc. Res., 20: 319.PubMedCrossRefGoogle Scholar
  21. Whereat, A.F., Mull, F.E., and Orishimo, M.W., 1967, The role of succinate in the regulation of fatty acid synthesis of heart mitochondria, J. Biol. Chem., 242: 4013.PubMedGoogle Scholar
  22. Wilson, D.F., Owen, C.S., and Erecinska, M., 1979, Quantitative dependence of mitochondrial oxidative phosphorylation on oxygen concentrations, Arch. Biochem. Biophys., 195: 495.Google Scholar

Copyright information

© Plenum Press, New York 1984

Authors and Affiliations

  • J. Moravec
    • 1
  • J. Nzonzi
    • 1
  • C. Bowe
    • 2
  • D. Feuvray
    • 2
  1. 1.I. N.S. E.R. M. U2Hopital Léon BernardLimeil-BrévannesFrance
  2. 2.Department of PhysiologyFaculté des SciencesOrsayFrance

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