Assessment of cardiac function and energetics in isolated mouse hearts using 31P NMR spectroscopy

Journal of Visualized Experiments

Volumn , Issue 42, 2010, Pages

  Kolwicz Jr , Stephen C ^a   Tian, Rong ^a  

^a UNIVERSITY OF WASHINGTON   (United States)

Author keywords

ATP; Cardiac physiology; High energy phosphate; Issue 42; Medicine; Phosphocreatine

Indexed keywords

EID: 80355140401     PISSN: 1940087X     EISSN: None     Source Type: Journal    
DOI: 10.3791/2069     Document Type: Article

References (12)

1. Nascimben, L., J.S. Ingwall, B.H. Lorell, I. Pinz, V. Schultz, K. Tornheim, & R. Tian. Mechanisms for increased glycolysis in the hypertrophied rat heart. Hypertension. 44, 662-667, (2004).
2. Spindler, M., K.W. Saupe, R. Tian, S. Ahmed, M.A. Matlib, & J.S. Ingwall. Altered creatine kinase enzyme kinetics in diabetic cardiomyopathy. A(31)P NMR magnetization transfer study of the intact beating rat heart. J Mol Cell Cardiol. 31, 2175-2189, (1999).
3. Ingwall, J.S. Phosphorus nuclear magnetic resonance spectroscopy of cardiac and skeletal muscles. Am J Physiol. 242, H729-H744, (1982).
4. Ingwall, J.S., Javadpour, M.M., and Miao, W. 31P NMR spectroscopy of the mouse heart, in Cardiovascular physiology in the genetically engineered mouse. B.D. Hoit, Walsh, R.A., Editor. Kluwer: Boston. 151-163 (2002).
5. Luptak, I., J.A. Balschi, Y. Xing, T.C. Leone, D.P. Kelly, & R. Tian. Decreased contractile and metabolic reserve in peroxisome proliferator-activated receptor-alpha-null hearts can be rescued by increasing glucose transport and utilization. Circulation. 112, 2339-2346, (2005).
6. Yan, J., M.E. Young, L. Cui, G.D. Lopaschuk, R. Liao, & R. Tian. Increased glucose uptake and oxidation in mouse hearts prevent high fatty acid oxidation but cause cardiac dysfunction in diet-induced obesity. Circulation. 119, 2818-2828, (2009).
7. Luptak, I., M. Shen, H. He, M.F. Hirshman, N. Musi, L.J. Goodyear, J. Yan, H. Wakimoto, H. Morita, M. Arad, C.E. Seidman, J.G. Seidman, J.S. Ingwall, J.A. Balschi, & R. Tian. Aberrant activation of AMP-activated protein kinase remodels metabolic network in favor of cardiac glycogen storage. J Clin Invest. 117, 1432-1439, (2007).
8. Xing, Y., N. Musi, N. Fujii, L. Zou, I. Luptak, M.F. Hirshman, L.J. Goodyear, & R. Tian. Glucose metabolism and energy homeostasis in mouse hearts overexpressing dominant negative alpha2 subunit of AMP-activated protein kinase. J Biol Chem. 278, 28372-28377, (2003).
9. Luptak, I., J. Yan, L. Cui, M. Jain, R. Liao, & R. Tian. Long-term effects of increased glucose entry on mouse hearts during normal aging and ischemic stress. Circulation. 116, 901-909, (2007).
10. Tian, R. and E.D. Abel. Responses of GLUT4-deficient hearts to ischemia underscore the importance of glycolysis. Circulation. 103, 2961-2966, (2001).
11. Liao, R., M. Jain, L. Cui, J. D'Agostino, F. Aiello, I. Luptak, S. Ngoy, R.M. Mortensen, & R. Tian. Cardiac-specific overexpression of GLUT1 prevents the development of heart failure attributable to pressure overload in mice. Circulation. 106, 2125-2131, (2002).
12. Tian, R., N. Musi, J. D'Agostino, M.F. Hirshman, & L.J. Goodyear. Increased adenosine monophosphate-activated protein kinase activity in rat hearts with pressure-overload hypertrophy. Circulation. 104, 1664-1669, (2001).