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31P-NMR magnetization transfer study of reperfused rat heart

  • Cellular Function and Metabolism
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Abstract

The relationships between pressure rate product (PRP) and flux(PCr → ATP) or flux(Pi → ATP) were studied in isolated perfused rat hearts by the method of saturation transfer using31P-NMR during the preischemic and reperfusion periods. The hearts were made ischemic for 15 min, followed by 60 min of reperfusion. PRP was almost completely depressed, and recovered to 60^ of the control level (preischemic period) after reperfusion. The ATP level during reperfusion was significantly decreased, whereas there was no significant change in PCr level. Pi level of reperfused hearts was significantly higher than that in the control. Both flux(PCr → ATP) and flux(Pi → ATP) were significantly decreased during the reperfusion period (both p<0.05). However, the flux(PCr → ATP)/PRP ratio during reperfusion did not differ from that of the control. This result indicates that the decrease in flux(PCr → ATP) was matched by a similar decrease in cardiac performance. In contrast, the flux(Pi → ATP)/PRP ratio during reperfusion was significantly decreased compared to that of control. These results suggest that the stunned heart needs less ATP turnover in proportion to its depressed contractile activity, and flux(Pi → ATP) may limit the recovery of postischemic performance.

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References

  1. Ambrosio G, Jacobus WE, Bergman CA, Weismann HF, Becker LC: Preserved high energy phosphate metabolic reserve in globally ‘stunned’ hearts despite reduction of basal ATP content and contractility. J Mol Cell Cardiol 19: 953–964, 1987

    Google Scholar 

  2. Neely JR, Grotyohann LW: Role of glycolytic products in damage to ischemic myocardium. Dissociation of adenosine triphosphate levels and recovery of function of reperfused ischemic hearts. Circ Res 55: 816–824, 1984

    Google Scholar 

  3. Zweier J, Jacobus WE: Substrate-induced alterations of high energy phosphate metabolism and contractile function in the perfused heart. J Biol Chem 262: 8015–8021, 1987

    Google Scholar 

  4. Bessman SP, Geiger PJ: Transport of energy in muscle: The phosphorylcreatine shuttle. Science 211: 448–452, 1981

    Google Scholar 

  5. Foresen S, Hoffman RA: Study of moderately rapid chemical exchange reactions by means of nuclear magnetic double resonance. J Chem Phys 39: 2892–2901, 1963

    Google Scholar 

  6. Nunnally RL, Hollis DP: Adenosine triphosphate compartmentation in living hearts: A phosphorus nuclear magnetic resonance saturation transfer study. Biochem 18: 3642–3646, 1979

    Google Scholar 

  7. Degani H, Laughlin M, Campbell S, Shulman RG: Kinetics of creatine kinase in heart: A31P NMR saturation- and inversion-transfer study. Biochem 24: 5510–5516, 1985

    Google Scholar 

  8. Bittl JA, Ingwall JS: Reaction rates of creatine kinase and ATP synthesis in the isolated rate heart. A31P NMR magnetization transfer study. J Biol Chem 260: 3512–3517, 1985

    Google Scholar 

  9. Bittl JA, Baischi JA, Ingwall JS: Effects of norepinephrine infusion on myocardial high-energy phosphate content and turnover in the living rat. J Clin Invest 79: 1852–1859, 1987

    Google Scholar 

  10. Neubauer S, uman BL, Perry SB, Bittl JA, Ingwall JS: Velocity of the creatine kinase reaction decreases in postischemic myocardium: A31P NMR magnetization transfer study of the isolated ferret heart. Circ Res 63: 1–15, 1988

    Google Scholar 

  11. Perry SB, McAuliffe J, Balschi JA, Hickey PR, Ingwall JS: Velocity of the creatine kinase reaction in the neonatal rabbit heart: Role of mitochondrial creatine kinase. Biochem 27: 2165–2172, 1988

    Google Scholar 

  12. Kobayashi K, Neely JR: Control of maximum rates of glycolysis in rat cardiac muscle. Circ Res 44: 166–175, 1979

    Google Scholar 

  13. Matthews PM, Bland JL, Gadian DG, Radda GK: A31P-NMR saturation transfer study of the regulation of creatine kinase in the rat heart. Biochim Biophys Acta 721: 312–320, 1982

    Google Scholar 

  14. Brindle KM, Radda GK:31P-NMR saturation transfer measurements of exchange between Pi and ATP in the reactions catalysed by glyceraldehyde-3-phosphate dehydro genase and phosphoglycerate kinasein vitro. Biochim Biophys Acta 928: 45–55, 1987

    Google Scholar 

  15. Ugurbil K, Petein M, Maidan R, Michurski S, From AHL: Measurement of an individual rate constant in the presence of multiple exchanges: Application to myocardial creatine kinase reaction. Biochem 25: 100–107, 1986

    Google Scholar 

  16. Seymour AML, Eldar H, Radda GK: Hyperthyroidism results in increased glycolytic capacity in the rat heart. A31P-NMR study. Biochim Biophys Acta 1055: 107–116, 1990

    Google Scholar 

  17. Brindle KM:31P NMR magnetization-transfer measurement of flux between inorganic phosphate and adenosine 5′-triphosphate in yeast cell genetically modified to overproduce phosphoglycerate kinase. Biochem 27: 6187–6196, 1988

    Google Scholar 

  18. Diederichs F, Wittenberg H, Sommerfield U: Myocardial cell damage and breakdown of cation homeostasis during conditions of ischaemia and reperfusion, the oxygen paradox, and reduced extracellular calcium. J Clin Chem Clin Biochem 28: 139–148, 1990

    Google Scholar 

  19. Piper HM, Sezer O, Schleyer M, Schwartz P, Hutter JF, Spieckermann PG: Development of ischemia-induced damage in defined mitochondrial subpopulations. J Mol Cell Cardiol 17: 885–896, 1985

    Google Scholar 

  20. Apstein CS, Deckelbaum L, Hagopian L, Hood WB: Acute ischemia and reperfusion: Contractility, relaxation and glycolysis. Am J Physiol 235: H637-H648, 1978

    Google Scholar 

  21. Bolli R: Mechanism of myocardial ‘stunning’. Circulation 82: 723–738, 1990

    Google Scholar 

  22. Kusuoka H, Koretune Y, Chacko VP, Weisfeldt ML, Marban E: Excitation-contraction coupling in postischemic myocardium. Circ Res 66: 1268–1276, 1990

    Google Scholar 

  23. Fabiato A, Fabiato F: Effects of pH on the myofilaments and the sarcoplasmic reticulum of skinned cells from cardiac skeletal muscles. J Physiol 276: 233–255, 1978

    Google Scholar 

  24. MacDonald TF, Hunter EG, Macleod DP: ATP partition in cardiac muscle with respect to transmembrane electrical activity. Pflugers Arch 322: 95–108, 1971

    Google Scholar 

  25. Niki I, Ashcroft FM, Ashcroft SJH: The dependence on intracellular ATP concentration of ATP-sensitive K-channels and of Na+,K+-ATPase in intact HIT-TI5 beta-cells. FBBS Lett 257: 361–364, 1989

    Google Scholar 

  26. Herzig JW, Peterson JW, Ruegg RJ, Solaro RJ: Vanadate and phosphate ions reduce tension and increase cross-bridge kinetics in chemically skinned heart muscle. Biochim Biophys Acta 672: 191–196, 1981.

    Google Scholar 

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Authors and Affiliations

  1. The Third Department of Internal Medicine, Hamamatsu University School of Medicine, 3600, Handa-cho, 431-31, Hamamatsu, Japan

    Akira Kobayashi, Yoshimi Okayama & Noboru Yamazaki

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  1. Akira Kobayashi
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  2. Yoshimi Okayama
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  3. Noboru Yamazaki
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Kobayashi, A., Okayama, Y. & Yamazaki, N. 31P-NMR magnetization transfer study of reperfused rat heart. Mol Cell Biochem 119, 121–127 (1993). https://doi.org/10.1007/BF00926862

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