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31P NMR Spectroscopy of the Mouse Heart

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Cardiovascular Physiology in the Genetically Engineered Mouse

Abstract

NMR spectroscopy of tissues and organs yields two kind of information: the steady state tissue content of abundant NMRobservable metabolites and ions and the kinetics of certain enzymes and metabolic pathways. Because these measurements are noninvasive, they can be made repetitively throughout a protocol. They can also be made simultaneously with assessment of physiologic function. In the case for 31P NMR spectroscopy of the isolated heart, and for the heart in situ, it is possible to make measurements of ATP and phosphocreatine (PCr) contents and turnover rates while simultaneously assessing systolic and diastolic performance. Such information is unique and provides a valuable solution to the perennial conflict between biochemistry and physiology. The biochemist dares to extrapolate results obtained from dilute solutions to the protein-rich cytosol, hoping that the results have functional meaning. The physiologist is so convinced of the importance of studying the intact heart, that he/she treats the heart as a black-box about which no molecular information can be known. The biophysicist has the best of both worlds: using NMR spectroscopy, one can learn about biochemical events within the cell while respecting the integrity of the physiological system.

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References

  1. Gadian DG. ed: NMR and its Applications to Living Systems, second edition. 1995; New York, Oxford University Press, Inc.

    Google Scholar 

  2. Ingwall JS. Phosphorus nuclear magnetic resonance spectroscopy of cardiac and skeletal muscle. Am J Physiol. 1982; 242:H729–H744.

    PubMed  CAS  Google Scholar 

  3. Ingwall JS, Weiss RG. 31P NMR Spectroscopy. The noninvasive tool for the study of the biochemistry of the cardiovascular system. Trends Cardiovasc Med. 1993; 3:29–37.

    Article  CAS  Google Scholar 

  4. Moon RB, Richards JH. Determination of intracellular pI-1 by 31P NMR. J Biol Chem. 1973; 248:7276–7278.

    PubMed  CAS  Google Scholar 

  5. Gupta RK. On the state of magnesium ion in intact cells as observed by noninvasive P-31 NMR spectroscopy. Int J Quantum Chem. 1980; 7:67–73.

    CAS  Google Scholar 

  6. Bittl JA, Ingwall JS. Reaction rates of creatine kinase and ATP synthesis in the isolated rat heart. J Biol Chem. 1985; 260(6):3512–3517.

    PubMed  CAS  Google Scholar 

  7. Freidrich J, Nascimben L, Liao R, Ingwall JS. Phosphocreatine T1 measurements with and without exchange in the heart. Magn Reson Med. 1993; 30:45–50.

    Article  Google Scholar 

  8. Chu G, Luo W, Slack JP, Tilgmann C, Sweet WE, Spindler M, Saupe KW, Boivin GP, Moravec CS, Matlib MA, Grupp IL, Ingwall JS, Kranias EG. Compensatory mechanisms associated with the hyperdynamic function of phospholamban-deficient mouse hearts. Circ Res. 1996; 78:1064–1076.

    Article  Google Scholar 

  9. Radford NB, Fina M, Benjamin IJ, Moreadith RW, Graves KH, Zhao P, Gavva S, Wiethoff A, Sherry AD, Malloy CR, Williams RS. Cardioprotective effects of 70-kDa heat shock protein in transgenic mice. Proc Natl Acad Sci U S A. 1996; 93(6):2339–42.

    Article  PubMed  CAS  Google Scholar 

  10. Saupe KW, Spindler M, Tian R, Ingwall JS. Impaired cardiac energetics in mice lacking muscle-specific isoenzymes of creatine kinase. Circ Res. 1998; 82:898–907.

    Article  PubMed  CAS  Google Scholar 

  11. Van Dorsten FA, Nederhoff MG, Nicolay K, Van Echteld CJ. 31P NMR studies of creatine kinase flux in M-creatine kinase-deficient mouseheart. Am J Physiol. 1998; 275(4 Pt 2):H1191–9.

    PubMed  Google Scholar 

  12. Saupe KW, Spindler M, Hopkins JC, Shen W, Ingwall JS. Kinetic, thermodynamic, and developmental consequences of deleting creatine kinase isoenzymes from the heart: reaction kinetics of the creatine kinase isoenzymes in the intact heart. J Biol Chem. 2000; 275(26):19742–19746.

    Article  PubMed  CAS  Google Scholar 

  13. Spindler M, Saupe KW, Christe ME, Sweeny HL, Seidman CE, Seidman JG, Ingwall JS. Diastolic dysfunction and altered energetics in the □MHC403/+ mouse model of familial hypertrophic cardiomyopathy. J Clin Invest. 1998; 101:1775–1783.

    Article  PubMed  CAS  Google Scholar 

  14. Tian R, Miao W, Spindler M, Javadpour MM, McKinney R, Bowman JC, Buttrick PM, Ingwall JS. Long-term expression of protein kinase C in adult mouse hearts improves postischemic recovery. Proc National Acad Sci. 1999; 96(23):13536–13541.

    Article  CAS  Google Scholar 

  15. Flogel U, Decking UK, Godecke A, Schrader J. Contribution of NO to ischemia-reperfusion injury in the saline-perfused heart: a study in endothelial NO synthase knockout mice. J Mol Cell Cardiol. 1999; (4):827–36.

    Article  Google Scholar 

  16. Godecke A, Flogel U, Zanger K, Ding Z, Hirchenhain J, Decking UK, Schrader J. Disruption of myoglobin in mice induces multiple compensatory mechanisms. Proc Natl Acad Sci USA. 1999; 96(18):10495–500.

    Article  PubMed  CAS  Google Scholar 

  17. Cross HR, Steenbergen C, Lefkowitz RJ, Koch WJ, Murphy E. Overexpression of the cardiac beta(2)-adrenergic receptor and expression of a beta-adrenergic receptor kinase 1 (betaARKI) inhibitor both increase myocardial contractility but have differential effects on susceptibility to ischemic injury. Circ Res. 1999; 85(11):1077–84.

    Article  PubMed  CAS  Google Scholar 

  18. Abel ED, Kaulbach HC, Tian R, Hopkins JCA, Duffy J, Doetschman T, Minnemann T, Boers M-E, Hadro E, Oberste-Berghaus C, Quist W, Lowell BB, Ingwall JS, Kahn BB. Cardiac hypertrophy with preserved contractile function after deletion of GLUT4 from the heart. J Clin Invest. 1999; 104(12):1703–1714.

    Article  PubMed  CAS  Google Scholar 

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© 2001 Springer Science+Business Media New York

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Ingwall, J.S., Javadpour, M.M., Miao, W. (2001). 31P NMR Spectroscopy of the Mouse Heart. In: Hoit, B.D., Walsh, R.A. (eds) Cardiovascular Physiology in the Genetically Engineered Mouse. Developments in Cardiovascular Medicine, vol 238. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1653-8_10

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  • DOI: https://doi.org/10.1007/978-1-4615-1653-8_10

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  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-5661-5

  • Online ISBN: 978-1-4615-1653-8

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