| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Departments of Medicine and Radiology, University of Minnesota Health Sciences, Minneapolis, Minnesota 55455; and 2 Centre de Génétique Moléculaire et Cellulaire, Centre National de la Recherche Scientifique Lyon I, 69622 Villeurbanne Cedex, France
This study examined high-energy phosphates (HEP) and
mitochondrial ATPase protein expression in hearts in which myocardial infarction resulted in either compensated left ventricular remodeling (LVR) or congestive heart failure (CHF). The response of HEP (measured via 31P magnetic resonance spectroscopy) to a modest
increase in the cardiac work state produced by dobutamine-dopamine
infusion and pacing (if needed) was examined in 17 pigs after left
circumflex coronary artery ligation (9 with LVR and 8 with CHF) and
compared with 7 normal pigs. In hearts with LVR, the baseline
phosphocreatine (PCr)-to-ATP ratio decreased, and calculated ADP
increased; these changes were most severe in hearts with CHF. HEP
levels did not change in normal or LVR hearts during
dobutamine-dopamine infusion. However, in hearts with CHF, the
PCr-to-ATP ratio decreased further, and free ADP increased. The
mitochondrial protein levels of the F0F1-ATPase
subunits were normal in hearts with compensated LVR. However, in
failing hearts, the 
-subunit decreased by 36%, the 
-subunit
decreased by 16%, the oligomycin sensitivity-conferring protein
subunit decreased by 40%, and the initiation factor 1 subunit
decreased by 41%. Thus in failing hearts, reductions in mitochondrial F0F1-ATPase protein expression
are associated with increased myocardial free ADP.
myocardial infarct; catecholamine; creatine kinase; phosphocreatine
This article has been cited by other articles:
|
|
 |
|
  M. van Bilsen, F. A. van Nieuwenhoven, and G. J. van der Vusse Metabolic remodelling of the failing heart: beneficial or detrimental? Cardiovasc Res, February 15, 2009; 81(3): 420 - 428. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. G. Rosca, E. J. Vazquez, J. Kerner, W. Parland, M. P. Chandler, W. Stanley, H. N. Sabbah, and C. L. Hoppel Cardiac mitochondria in heart failure: decrease in respirasomes and oxidative phosphorylation Cardiovasc Res, October 1, 2008; 80(1): 30 - 39. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. J. Eisen Exercise Training and Myocardial Energetics in Patients With Heart Failure: When More Is Less J. Am. Coll. Cardiol., May 13, 2008; 51(19): 1892 - 1895. [Full Text] [PDF]
|
|
|
|
 |
|
 J. Feygin, Q. Hu, C. Swingen, and J. Zhang Relationships between regional myocardial wall stress and bioenergetics in hearts with left ventricular hypertrophy Am J Physiol Heart Circ Physiol, May 1, 2008; 294(5): H2313 - H2321. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Feygin, A. Mansoor, P. Eckman, C. Swingen, and J. Zhang Functional and bioenergetic modulations in the infarct border zone following autologous mesenchymal stem cell transplantation Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1772 - H1780. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Zeng, Q. Hu, X. Wang, A. Mansoor, J. Lee, J. Feygin, G. Zhang, P. Suntharalingam, S. Boozer, A. Mhashilkar, et al. Bioenergetic and Functional Consequences of Bone Marrow-Derived Multipotent Progenitor Cell Transplantation in Hearts With Postinfarction Left Ventricular Remodeling Circulation, April 10, 2007; 115(14): 1866 - 1875. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Neubauer The Failing Heart -- An Engine Out of Fuel N. Engl. J. Med., March 15, 2007; 356(11): 1140 - 1151. [Full Text] [PDF]
|
|
|
|
|
|
Q. Hu, X. Wang, J. Lee, A. Mansoor, J. Liu, L. Zeng, C. Swingen, G. Zhang, J. Feygin, K. Ochiai, et al. Profound bioenergetic abnormalities in peri-infarct myocardial regions Am J Physiol Heart Circ Physiol, August 1, 2006; 291(2): H648 - H657. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Wallis, C. A. Lygate, A. Fischer, M. ten Hove, J. E. Schneider, L. Sebag-Montefiore, D. Dawson, K. Hulbert, W. Zhang, M. H. Zhang, et al. Supranormal Myocardial Creatine and Phosphocreatine Concentrations Lead to Cardiac Hypertrophy and Heart Failure: Insights From Creatine Transporter-Overexpressing Transgenic Mice Circulation, November 15, 2005; 112(20): 3131 - 3139. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. C. Stanley, F. A. Recchia, and G. D. Lopaschuk Myocardial Substrate Metabolism in the Normal and Failing Heart Physiol Rev, July 1, 2005; 85(3): 1093 - 1129. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. M. Regula, M. J. Rzeszutek, D. Baetz, C. Seneviratne, and L. A. Kirshenbaum Therapeutic opportunities for cell cycle re-entry and cardiac regeneration Cardiovasc Res, December 1, 2004; 64(3): 395 - 401. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. V. Gourine, Q. Hu, P. R. Sander, A. I. Kuzmin, N. Hanafy, S. A. Davydova, D. V. Zaretsky, and J. Zhang Interstitial purine metabolites in hearts with LV remodeling Am J Physiol Heart Circ Physiol, February 1, 2004; 286(2): H677 - H684. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. P. Czubryt and E. N. Olson Balancing Contractility and Energy Production: The Role of Myocyte Enhancer Factor 2 (MEF2) in Cardiac Hypertrophy Recent Prog. Horm. Res., January 1, 2004; 59(1): 105 - 124. [Abstract] [Full Text]
|
|
|
|
|
|
G. Gong, J. Liu, P. Liang, T. Guo, Q. Hu, K. Ochiai, M. Hou, Y. Ye, X. Wu, A. Mansoor, et al. Oxidative capacity in failing hearts Am J Physiol Heart Circ Physiol, July 11, 2003; 285(2): H541 - H548. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
X.-H. Ning, S.-H. Chen, C.-S. Xu, O. M. Hyyti, K. Qian, J. J. Krueger, and M. A. Portman Hypothermia preserves myocardial function and mitochondrial protein gene expression during hypoxia Am J Physiol Heart Circ Physiol, June 5, 2003; 285(1): H212 - H219. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
