31P NMR Spectroscopy of the Mouse Heart
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.
KeywordsNuclear Magnetic Resonance Nuclear Magnetic Resonance Spectroscopy Mouse Heart Nuclear Magnetic Resonance Experiment Cardiovascular Physiology
Unable to display preview. Download preview PDF.
- 1.Gadian DG. ed: NMR and its Applications to Living Systems, second edition. 1995; New York, Oxford University Press, Inc.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.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.PubMedCrossRefGoogle 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.PubMedCrossRefGoogle 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.PubMedCrossRefGoogle Scholar