Failing energetics in failing hearts

Current Cardiology Reports

Volumn 2, Issue 3, 2000, Pages 212-217

  Dzeja, Petras P ^a   Redfield, Margaret M ^a   Burnett, John C ^a   Terzic, Andre ^a  

^a MAYO CLINIC   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ADENOSINE TRIPHOSPHATE; CREATINE KINASE;

ANIMAL; CONGESTIVE HEART FAILURE; ENERGY METABOLISM; GLYCOLYSIS; HEART MUSCLE; HUMAN; METABOLISM; PHOSPHORYLATION; PHYSIOLOGY; REVIEW;

ADENOSINE TRIPHOSPHATE; ANIMALS; CREATINE KINASE; ENERGY METABOLISM; GLYCOLYSIS; HEART FAILURE, CONGESTIVE; HUMANS; MYOCARDIUM; PHOSPHORYLATION;

EID: 0034183982     PISSN: 15233782     EISSN: 15343170     Source Type: Journal    
DOI: 10.1007/s11886-000-0071-9     Document Type: Article

References (52)

1. Ingwall JS: Is cardiac failure a consequence of decreased energy reserve? Circulation 1993, 87:VII58-VII62.
2. Taegtmeyer H: Energy metabolism of the heart: from basic concepts to clinical applications. Curr Probl Cardiol 1994, 19:59-113.
3. Opie LH: Substrate and energy metabolism in the heart. In Physiology and pathophysiology of the heart. Edited by Sperelakis N. Boston: Kluwer; 1995:367-384.
4. Saks VA, Tiivel T, Kay L, et al. : On the regulation of cellular energetics in health and disease. Mol Cell Biochem 1996, 160-161:195-208.
5. Schwartz K, Mercadier JJ: Molecular and cellular biology of heart failure. Curr Opin Cardiol 1996, 11:227-236.
6. Mittmann C, Eschenhagen T, Scholz H: Cellular and molecular aspects of contractile dysfunction in heart failure. Cardiovasc Res 1998, 39:267-75.
7. Shen WQ, Asai K, Uechi M, et al. : Progressive loss of myocardial ATP due to a loss of total purines during the development of heart failure in dogs-a compensatory role for the parallel loss of creatine. Circulation 1999, 100:2113-2118.
8. Tian R, Ingwall JS: Energetic basis for reduced contractile reserve in isolated rat hearts. Am J Physiol 1996, 270:H1207-H1216.
9. Jennings RB, Murry CE, Reimer KA: Energy metabolism in preconditioned and control myocardium: effect of total ischemia. J Mol Cell Cardiol 1991, 23:1449-1458.
10. Hassinen IE, Vuorinen KH, Ylitalo K, et al. : Role of cellular energetics in ischemia-reperfusion and ischemic preconditioning of myocardium. Mol Cell Biochem 1998, 184:393-400.
11. Kloner RA, Bolli R, Marban E, et al. : Medical and cellular implications of stunning, hibernation, and preconditioning. Circulation 1998, 97:1848-1867.
12. Dzeja PP, Pucar D, Redfield MM, et al. : Reduced activity of enzymes coupling ATP-generating with ATP-consuming processes in the failing myocardium. Mol Cell Biochem 1999, 201:33-40.
13. Taegtmeyer H, Goodwin GW, Doenst T, et al. : Substrate metabolism as determinant for post-ischemic functional recovery of the heart. Am J Cardiol 1997, 80:3A-10A.
14. Lewandowski ED, Yu X, LaNoue KF, et al. : Altered metabolite exchange between subcellular compartments in intact post-ischemic rabbit hearts. Circ Res 1997, 81:165-175.
15. Zuurbier CJ, van Beek JHGM: Mitochondrial response to heart rate steps in isolated rabbit heart is slowed after myocardial stunning. Circ Res 1997, 81:69-75.
16. Dzeja PP, Zeleznikar RJ, Goldberg ND: Adenylate kinase: kinetic behavior in intact cells indicates it is integral to multiple cellular processes. Mol Cell Biochem 1998, 84:169-182.
17. Dzeja PP, Terzic A: Phosphotransfer reactions in the regulation of ATP-sensitive K+ channels. FASEB J 1998, 12:523-529.
18. Wiese S, Katz DP, Manner T, et al. : Impact of specific substrate supply on efficiency of cardiac function: an update. Nutrition 1993, 9:495-506.
19. Takahashi E, Doi K: Regulation of oxygen diffusion in hypoxic isolated cardiac myocytes. Am J Physiol 1996, 271:H1734-H1738.
20. Godecke A, Flogel U, Zanger K, et al. : Disruption of myoglobin in mice induces multiple compensatory mechanisms. Proc Natl Acad Sci U S A 1999, 96:10495-10500.
21. Weil J, Eschenhagen T, Magnussen O, et al. : Reduction of myocardial myoglobin in bovine dilated cardiomyopathy. J Mol Cell Cardiol 1997, 29:743-751.
22. Heinke MY, Wheeler CH, Yan JX, et al. : Changes in myocardial protein expression in pacing-induced canine heart failure. Electrophoresis 1999, 20:2086-2093.
23. Kammermeier H, Wein B, Gerards P, et al. : Barriers in cardiac substrate supply. Bas Res Cardiol 1985, 80:89-92.
24. Auffermann W, Wu ST, Parmley WW, et al. : Glycolysis in heart failure: A 31P-NMR and surface fluorometry study. Bas Res Cardiol 1990, 85:342-357.
25. Askenasy N, Navon G: Intermittent ischemia-energy metabolism, cellular volume regulation, adenosine and insights into preconditioning. J Mol Cell Cardiol 1997, 29:1715-1730.
26. Stanley WC, Lopaschuk GD, Hall JL, McCormack JG: Regulation of myocardial carbohydrate metabolism under normal and ischaemic conditions. Potential for pharmacological interventions. Cardiovasc Res 1997, 33:243-257.
27. Regitz V, Fleck E: Myocardial adenine nucleotide concentrations and myocardial norepinephrine content in patients with heart failure secondary to idiopathic dilated or ischemic cardiomyopathy. Am J Cardiol 1992, 69: 1574-1580.
28. McDonald KM, Yoshiyama M, Francis GS, et al. : Myocardial bioenergetic abnormalities in a canine model of left ventricular dysfunction. J Am Coll Cardiol 1994, 23:786-793.
29. Pouleur H, Hayashida W: Diastolic dysfunction and myocardial energetics. In Diastolic relaxation of the heart. Edited by Lorell BH, Grossman, W. Boston: Kluwer; 1994:277-282.
30. Neubauer S, Horn M, Cramer M, et al. : Myocardial phosphocreatine-to-ATP ratio is a predictor of mortality in patients with dilated cardiomyopathy. Circulation 1997, 96:2190-2196.
31. Cohn JN, Bristow MR, Chien KR, et al. : Report of the National Heart, Lung, and Blood Institute Special Emphasis Panel on Heart Failure Research. Circulation 1997, 95:766-770.
32. Dzeja PP, Vitkevicius KT, Redfield MM, et al. : Adenylate kinasecatalyzed phosphotransfer in the myocardium: increased contribution in heart failure. Circ Res 1999, 84:1137-1143.
33. O'Brien PJ, Gwathmey JK: Myocardial Ca2+-and ATP-cycling imbalances in end-stage dilated and ischemic cardiomyopathies. Cardiovasc Res 1995, 30:394-404.
34. Heinke MY, Wheeler CH, Chang D, et al. : Protein changes observed in pacing-induced heart failure using two-dimensional electrophoresis. Electrophoresis 1998, 19:2021-2030.
35. Hayashi Y, Takeuchi M, Takaoka H, et al. : Alteration in energetics in patients with left ventricular dysfunction after myocardial infarction: increased oxygen cost of contractility. Circulation 1996, 93:932-939.
36. Panagia V, Lee SL, Singh A, et al. : Impairment of mitochondrial and sarcoplasmic reticular functions during the development of heart failure in cardiomyopathic (UM-X7. 1) hamsters. Can J Cardiol 1986, 2:236-247.
37. Katz AM: Energy requirements of contraction and relaxation: implications for inotropic stimulation of the failing heart. Bas Res Cardiol 1989, 84:47-53.
38. Kalsi KK, Smolenski RT, Pritchard RD, et al. : Energetics and function of the failing human heart with dilated or hypertrophic cardiomyopathy. Eur J Clin Invest 1999, 29:469-477.
39. Kluck RM, Bossy-Wetzel E, Green DR, Newmeyer DD: The release of cytochrome c from mitochondria: a primary site for bcl-2 regulation of apoptosis. Science 1997, 275:1132-1136.
40. Olivetti G, Abbi R, Quaini F, et al. : Apoptosis in the failing human heart. N Engl J Med 1997, 336:1131-1141.
41. Ottaway JH, Mowbray J: The role of compartmentation in the control of glycolysis. Curr Top Cell Reg 1977, 12:107-208.
42. Wallimann T, Wyss M, Brdiczka D, et al. : Intracellular compartmentation, structure and function of creatine kinase isoenzymes in tissues with high and fluctuating energy demands: the "phosphocreatine circuit" for cellular energy homeostasis. Biochem J 1992, 28:21-40.
43. van Deursen J, Heerschap A, Oerlemans F, et al. : Skeletal muscle of mice deficient in muscle creatine kinase lack burst activity. Cell 1993, 74:621-631.
44. Tian R, Christe ME, Spindler M, et al. : Role of MgADP in the development of diastolic dysfunction in the intact beating rat heart. J Clin Invest 1997, 99:745-751.
45. Veksler VI, Kuznetsov AV, Anflous K, et al. : Muscle creatine kinase-deficient mice. Cardiac and skeletal muscles exhibit tissue-specific adaptation of the mitochondrial function. J Biol Chem 1995, 270:19921-19929.
46. Dzeja PP, Zeleznikar RJ, Goldberg ND: Suppression of creatine kinase-catalyzed phosphotransfer results in increased phosphoryl transfer by adenylate kinase in intact skeletal muscle. J Biol Chem 1996, 271:12847-12851.
47. 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.
48. Steeghs K, Benders A, Oerlemans F, et al. : Altered Ca2+ responses in muscles with combined mitochondrial and cytosolic creatine kinase deficiencies. Cell 1997, 89:93-103.
49. Nascimben L, Ingwall JS, Pauletto P, et al. : Creatine kinase system in failing and nonfailing human myocardium. Circulation 1996, 94:1894-1901.
50. Soboll S, Brdiczka D, Jahnke D, et al. : Octamer-dimer transitions of mitochondrial creatine kinase in heart disease. J Mol Cell Cardiol 1999, 31:857-866.
51. Robitaille PM, Merkle H, Sako E, et al. : Measurement of ATP synthesis rates by 31P-NMR spectroscopy in the intact myocardium in vivo. Mag Res Med 1990, 15:8-24.
52. Gros G, Moll W, Hoppe H, Gros H: Proton transport by phosphate diffusion: A mechanism of facilitated CO2 transfer. J Gen Physiol 1976, 67:773-790.