Reduced inotropic reserve and increased susceptibility to cardiac ischemia/reperfusion injury in phosphocreatine-deficient guanidinoacetate-N-methyltransferase-knockout mice.

Journal article

BACKGROUND: The role of the creatine kinase (CK)/phosphocreatine (PCr) energy buffer and transport system in heart remains unclear. Guanidinoacetate-N-methyltransferase-knockout (GAMT-/-) mice represent a new model of profoundly altered cardiac energetics, showing undetectable levels of PCr and creatine and accumulation of the precursor (phospho-)guanidinoacetate (P-GA). To characterize the role of a substantially impaired CK/PCr system in heart, we studied the cardiac phenotype of wild-type ...

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Authors: ten Hove, M; Lygate, C; Fischer, A; Schneider, J; Sang, A

• Publication status: Published
• Journal: Circulation
• Volume: 111
• Issue: 19
• Pages: 2477-2485
• Publication date: 2005-05-01
• DOI: 10.1161/01.cir.0000165147.99592.01
• EISSN: 1524-4539
• ISSN: 0009-7322
• Language: English
• Keywords: Creatine Kinase; Guanidinoacetate N-Methyltransferase; Mice; Energy Metabolism; Myocardial Contraction; Stress, Physiological; Mice, Knockout; Cardiomegaly; Hemodynamics; Disease Susceptibility; Phosphocreatine; Myocardial Reperfusion Injury; Animals; Heart Function Tests; Myocardial Ischemia