Cardiology pp 583-595 | Cite as

Nuclear Magnetic Resonance Studies of Intracellular pH and Myocardial Contractility during Ischemia

  • William E. Jacobus
  • Clayton H. Kallman
  • Myron L. Weisfeldt
  • John T. Flaherty

Abstract

Most investigators in the field of molecular cardiology define myocardial ischemia in terms of a metabolic supply demand imbalance. Normal cell function is observed when supply is equal to or greater than demand. However, if coronary flow is reduced such that oxygen supply cannot meet the metabolic demands for the aerobic production of ATP (and phosphocreatine), then there must be a reduction in cell function1. In other words, cell function is in a delicate balance between metabolic (energetic) supply and its physiological demands, as illustrated by Equation 1.

Keywords

Perfusion Pressure Coronary Flow Coronary Blood Flow Myocardial Contractility Oxygen Utilization 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    R. B. Jennings, Relationship of acute ischemia to functional defects and irreversibility, Circ. 53, Suppl I: I-26 (1976).Google Scholar
  2. 2.
    A. M. Katz. Effects of ischemia on the contractile processes of heart muscle, Am. J. Card. 32: 456 (1973).PubMedCrossRefGoogle Scholar
  3. 3.
    W. Kubier and A. M. Katz. Mechanism of early “pump” failure of the ischemic heart. Possible role of adenosine triphosphate depletion and inorganic phosphate accumulation, Am. J. Card. 40:467 (1977).CrossRefGoogle Scholar
  4. 4.
    S. F. Khuri, J. T. Flaherty, J. B. O’Riordan, B. Pitt, R. K. Brawley, J. S. Donahoo and V. L. Gott. Changes in intramyo-cardial ST segment voltage and gas tensions with regional myocardial ischemia in the dog, Circ. Res. 37:455 (1975).PubMedCrossRefGoogle Scholar
  5. 5.
    W. E. Jacobus, I. H. Pores, S. K. Lucas, C. H. Kallman, M. L. Weisfeldt and J. T. Flaherty. The role of intracellular pH in the control of normal and ischemic myocardial contractility; a 31-P nuclear magnetic resonance and mass spectrometry study, in: “Intracellular pH: Its measurement, regulation and utilization in cellular functions”, R. Nuccitelli and D. W. Deamer, eds., Alan R. Liss, New York, 537 (1982).Google Scholar
  6. 6.
    D. G. Gadian, G. K. Radda, M. J. Dawson and D. R. Wilkie. pHi measurements of cardiac and skeletal muscle using 31-P NMR, in: “Intracellular pH: Its measurement, regulation and utilization in cellular functions”, R. Nuccitelli and D. W. Deamer, eds., Alan R. Liss, New York, 61 (1982).Google Scholar
  7. 7.
    R. J. Gillies, J. R. Alga, J. A. den Hollander and R. G. Shulman. Intracellular pH measured by NMR: Methods and results, in: “Intracellular pH : Its measurement, regulation and utilization in cellular functions”, R. Nuccitelli and D. W. Deamer, eds., Alan R. Liss, New York, 79 (1982).Google Scholar
  8. 8.
    S. F. Khuri, J. B. O’Riordan, J. T. Flaherty, R. K. Brawley, J. S. Donahoo and V. L. Gott. Mass spectrometry for the measurement of intramyocardial gas tensions: Methodology and application to the study of myocardial ischemia, in: “Recent Advances in Studies on Cardiac Structure and Metabolism, Vol. 10: Metabolism of Contraction”, T. E. Roy and G. Rona, eds., University Park Press, Baltimore, 539 (1975).Google Scholar
  9. 9.
    J. R. Neely and H. E. Morgan. Relationship between carbohydrate and lipid metabolism and the energy balance of heart muscle, Ann. Rev. Physiol. 36: 413 (1974).CrossRefGoogle Scholar
  10. 10.
    W. E. Jacobus, J. A. Bittl and M. L. Weisfeldt. Loss of mitochondrial creatine kinase in vitro and in vivo. A sensitive index of ischemic cellular and functional damage, in: “Heart creatine kinase: The integration of isozymes for energy distribution”, W. E. Jacobus and J. S. Ingwall, eds., Williams and Wilkins, Baltimore, 155 (1980).Google Scholar
  11. 11.
    A. Mukherjee, T. M. Wong, G. Templeton, L. M. Buja and J. T. Willerson. Influence of volume dilution, lactate, phosphate and calcium on mitochondrial functions, Am. J. Physiol. 237: H 224 (1979).Google Scholar
  12. 12.
    C. A. Apstein, J. Ahn, L. Briggs and H. M. Shapiro. Role of decrease in wall thickness in causing ischemic cardiac failure, Clin. Res. 27:436a (1979).Google Scholar
  13. 13.
    P. F. Salisburg, C. E. Cross and P. A. Rieben. Influence of coronary artery pressure upon myocardial elasticity, Circ. Res. 8:794 (1960).CrossRefGoogle Scholar
  14. 14.
    P. F. Salisburg, C. E. Cross and P. A. Rieben. Intramyocardial pressure and strength of left ventricular contraction, Circ. Res. 10:608 (1962).CrossRefGoogle Scholar
  15. 15.
    G. Arnold, F. Kosche, E. Miessner, A. Neitzert and W. Lochner. The importance of CK perfusion pressure in the coronary arteries for the contractility and oxygen consumption of the heart, Pfluegers Archiv. 299:339 (1968).CrossRefGoogle Scholar
  16. 16.
    B. N. Brent and C. S. Apstein. Kinetics of acute cardiac failure. Comparisons of ischemia, hypoxemia and cyanide, Clin. Res. 27: 156a (1979)Google Scholar
  17. 17.
    B. I. Jugdutt, L. C. Becker and G. M. Hutchins. Early changes in collateral blood flow during myocardial infarction in conscious dogs, Am. J. Physiol. 237(3):H371 (1979).Google Scholar

Copyright information

© Springer Science+Business Media New York 1984

Authors and Affiliations

  • William E. Jacobus
    • 1
    • 2
  • Clayton H. Kallman
    • 1
  • Myron L. Weisfeldt
    • 1
  • John T. Flaherty
    • 1
  1. 1.Department of MedicineThe John Hopkins University School of MedicineBaltimoreUSA
  2. 2.Department of Physiological ChemistryThe John Hopkins University School of MedicineBaltimoreUSA

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