Modest actomyosin energy conservation increases myocardial postischemic function

American Journal of Physiology - Heart and Circulatory Physiology

Volumn 288, Issue 3 57-3, 2005, Pages

  Blunt, Bradford C ^b   Chen, Yi ^b   Potter, James D ^a   Hofmann, Polly A ^b  

^a UNIVERSITY OF MIAMI MILLER SCHOOL OF MEDICINE   (United States)

^b UNIVERSITY OF TENNESSEE HEALTH SCIENCE CENTER   (United States)

Author keywords

Adenine nucleotides; Adenosinetriphosphatase; Hypothyroid; Left ventricular developed pressure; Preconditioning; Troponin T

Indexed keywords

ADENOSINE TRIPHOSPHATE; CARDIAC MYOSIN; MYOSIN ADENOSINE TRIPHOSPHATASE; MYOSIN HEAVY CHAIN BETA; PROPYLTHIOURACIL; PROTEIN KINASE C EPSILON; TROPONIN T; UNCLASSIFIED DRUG;

ACTIN MYOSIN INTERACTION; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; CONVALESCENCE; DOSE TIME EFFECT RELATION; ENERGY CONSERVATION; ENZYME ACTIVATION; ENZYME ACTIVITY; FEMALE; HEART FUNCTION; HEART INFARCTION PREVENTION; HEART LEFT VENTRICLE PRESSURE; HEART MUSCLE CONTRACTILITY; HEART MUSCLE ISCHEMIA; MALE; MOUSE; NONHUMAN; POINT MUTATION; PRIORITY JOURNAL; RAT; TRANSGENIC MOUSE;

ACTOMYOSIN; ADENINE; ADENOSINE TRIPHOSPHATASES; ADENOSINE TRIPHOSPHATE; ANIMALS; CALCIUM; CREATINE; ENERGY METABOLISM; FEMALE; HUMANS; HYPOTHYROIDISM; MALE; MICE; MICE, TRANSGENIC; MYOCARDIAL ISCHEMIA; MYOCARDIUM; MYOSIN HEAVY CHAINS; PROTEIN KINASE C; PROTEIN KINASE C-DELTA; PROTEIN KINASE C-EPSILON; RATS; RATS, SPRAGUE-DAWLEY; TROPONIN T;

EID: 13944277135     PISSN: 03636135     EISSN: None     Source Type: Journal    
DOI: 10.1152/ajpheart.00746.2004     Document Type: Article

References (35)

1. Abe M, Obata H, and Tanaka H. Functional and metabolic responses to ischemia in the isolated perfused hypothyroid rat heart. Jpn Circ J 56: 671-680, 1992.
2. Auchampach JA, Grover GJ, and Gross GJ. Blockade of ischaemic preconditioning in dogs by the novel ATP-dependent potassium channel antagonist sodium 5-hydroxydecanoate. Cardiovasc Res 26: 1054-1062, 1992.
3. 1-adrenergic mechanism. Circ Res 73: 656-670, 1993.
4. Benjamin IJ and McMillan DR. Stress (heat shock) proteins: molecular chaperones in cardiovascular biology and disease. Circ Res 83: 117-132, 1998.
5. Daly JA and Ertingshausen G. Direct method for determining inorganic phosphorus in serum with the Centrifuchem. Clin Chem 18: 263, 1972.
6. Ebus JP and Stienen GJ. Effects of 2,3-butanedione monoxime on cross-bridge kinetics in rat cardiac muscle. Pflügers Arch 432: 921-929, 1996.
7. Forbes RA, Steenbergen C, and Murphy E. Diazoxide-induced cardioprotection requires signalling through a redox-sensitive mechanism. Circ Res 88: 802-809, 2001.
8. Fralix TA, Murphy E, London RE, and Steenbergen C. Protective effects of adenosine in the perfused rat heart: changes in metabolism and intracellular ion homeostasis. Am J Physiol Cell Physiol 264: C986-C994, 1993.
9. + channels: possible mechanism of cardioprotection. Circ Res 81: 1072-1082, 1997.
10. Haist JV, Hirst CN, and Karmazyn M. Effective protection by NHE-1 inhibition in the ischemic and reperfused heart under preconditioning blockade. Am J Physiol Heart Circ Physiol 284: H798-H803, 2003.
11. Hoh JFY, McGrath PA, and Hale PT. Electrophoretic analysis of multiple forms of rat cardiac myosin: effects of hypophysectomy and thyroxine replacement. J Mol Cell Cardiol 10: 1053-1076, 1977.
12. Knollmann BC and Potter JD. Altered regulation of cardiac muscle contraction by troponin T mutations that cause familial hypertrophic cardiomyopathy. Trends Cardiovasc Med 11: 206-212, 2001.
13. Lebuffe G, Schumacker PT, Shao ZH, Anderson T, Iwase H, and Vanden Hoek TL. ROS and NO trigger early preconditioning: relationship to mitochondrial KATP channel. Am J Physiol Heart Circ Physiol 284: H299-H308, 2003.
14. Lester JW and Hofmann PA. Role for PKC in the adenosine-induced decrease in shortening velocity of rat ventricular myocytes. Am J Physiol Heart Circ Physiol 279: H2685-H2693, 2000.
15. Lopez-Torres M, Romero M, and Barja G. Effect of thyroid hormones on mitochondrial oxygen free radical production and DNA oxidative damage in the rat heart. Mol Cell Endocrinol 168: 127-134, 2000.
16. Miller T, Szczesna D, Housmans PR, Zhao J, de Freitas F, Gomes AV, Culbreath L, McCue J, Wang Y, Xu Y, Kerrick WGL, and Potter JD. Abnormal contractile function in transgenic mice expressing a familial hypertrophic cardiomyopathy-linked troponin T (179N) mutation. J Biol Chem 276: 3743-3755, 2001.
17. Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation 74: 1124-1136, 1986.
18. Noland TA Jr, Raynor RL, Jideama NM, Guo X, Kazanietz MG, Blumberg PM, Solaro RJ, and Kuo JF. Differential regulation of cardiac actomyosin S-I MgATPase by protein kinase C isozyme-specific phosphorylation of specific sites in cardiac troponin I and its phosphorylation site mutants. Biochemistry 35: 14923-14931, 1996.
19. Ohga Y, Susumu S, Takenaka C, Abe T, Tsuji T, Taniguchi S, and Takaki M. Cardiac dysfunction in terms of left ventricular mechanical work and energetics in hypothyroid rats. Am J Physiol Heart Circ Physiol 283: H631-H641, 2002.
20. Oliver IT. A spectrophotometric method for determination of creatine phosphokinase and myokinase. Biochemistry 61: 116, 1955.
21. O'Rourke B. Myocardial KATP channels in preconditioning. Circ Res 87: 845-855, 2000.
22. Pantos C, Malliopoulou V, Mourouzis I, Sfakianoudis K, Tzeis S, Doumba P, Xinaris C, Cokkinos AD, Carageorgiou H, Varonos DD, and Cokkinos DV. Propylthiouracil-induced hypothyroidism is associated with increased tolerance of the isolated rat heart to ischaemia-reperfusion. J Endocrinol 178: 427-435, 2003.
23. Pyle WG, Chen Y, and Hofmann PA. Cardioprotection through a PKC-dependent decrease in myofilament ATPase. Am J Physiol Heart Circ Physiol 285: H1220-H1228, 2003.
24. Quieroz MS, Shao Y, Berkich DA, Lanoue KF, and Ismail-Beigi F. Thyroid hormone regulation of cardiac bioenergetics: role of intracellular creatine. Am J Physiol Heart Circ Physiol 283: H2527-H2533, 2002.
25. Rajashree R, Koster JC, Markova KP, Nichols CG, and Hofmann PA. Contractility and ischemic response of hearts from transgenic mice with altered sarcolemmal KATP channels. Am J Physiol Heart Circ Physiol 283: H584-H590, 2002.
26. Reimer KA. The slowing of ischemic energy demand in preconditioned myocardium. Ann NY Acad Sci 793: 13-26, 1996.
27. Reiser PJ and Kline WO. Electrophoretic separation and quantitation of cardiac myosin heavy chain isoforms in eight mammalian species. Am J Physiol Heart Circ Physiol 274: H1048-H1053, 1998.
28. Roti E, Bandini P, Robuschi G, Emanuele R, Bolognesi R, Ciarlini E, Buzzonetti P, and Gnudi A. Serum concentrations of myoglobin, creatine kinase, lactate dehydrogenase, and cardiac isoenzymes in euthyroid, hypothyroid, and hyperthyroid subjects. Ric Clin Lab 10: 609-617, 1980.
29. 2+ transporters by thyroid hormone. Mol Cell Biochem 129: 145-159, 1993.
30. Suzuki M, Saito T, Sato T, Tamagawa M, Miki T, Seino S, and Nakaya H. Cardioprotective effect of diazoxide is mediated by activation of sarcolemmal but not mitochondrial ATP-sensitive potassium channels in mice. Circulation 107: 682-685, 2003.
31. Szczesna D, Zhang R, Zhao J, Jones M, Guzman G, and Potter JD. Altered regulation of cardiac muscle contraction by troponin T mutations that cause familial hypertrophic cardiomyopathy. J Biol Chem 275: 624-630, 2000.
32. Teerlink T, Hennekes M, Bussemaker J, and Groeneveld J. Simultaneous determination of. creatine compounds and adenine nucleotides in myocardial tissue by high-performance liquid chromatography. Anal Biochem 214: 278-283, 1993.
33. Tian R, Nascimben L, Kaddurah-Daouk R, and Ingwall JS. Depletion of energy reserve via the creatine kinase reaction during the evolution of heart failure in cardiomyopathic hamsters. J Mol Cell Cardiol 28: 755-765, 1996.
34. Tobacman LS, Lin D, Butters C, Landis CM, Back N, Pavlov D, and Homsher E. Functional consequences of troponin T mutations found in hypertrophic cardiomyopathy. J Biol Chem 274: 28363-28370, 1999.
35. 2+ sensitization and potentiation of the maximum level of myofibrillar ATPase activity caused by mutations of troponin T found in familial hypertrophic cardiomyopathy. J Biol Chem 26: 8806-8812, 1999.