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

Standard

Reduced inotropic reserve and increased susceptibility to cardiac ischemia/reperfusion injury in phosphocreatine-deficient guanidinoacetate-N-methyltransferase-knockout mice. / Michiel, Ten Hove; Lygate, Craig A; Fischer, Alexandra; Schneider, Jürgen E; Sang, A Elisabeth; Hulbert, Karen; Sebag-Montefiore, Liam; Watkins, Hugh; Clarke, Kieran; Isbrandt, Dirk; Wallis, Julie; Neubauer, Stefan.

in: CIRCULATION, Jahrgang 111, Nr. 19, 19, 2005, S. 2477-2485.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Michiel, TH, Lygate, CA, Fischer, A, Schneider, JE, Sang, AE, Hulbert, K, Sebag-Montefiore, L, Watkins, H, Clarke, K, Isbrandt, D, Wallis, J & Neubauer, S 2005, 'Reduced inotropic reserve and increased susceptibility to cardiac ischemia/reperfusion injury in phosphocreatine-deficient guanidinoacetate-N-methyltransferase-knockout mice.', CIRCULATION, Jg. 111, Nr. 19, 19, S. 2477-2485. <http://www.ncbi.nlm.nih.gov/pubmed/15883212?dopt=Citation>

APA

Michiel, T. H., Lygate, C. A., Fischer, A., Schneider, J. E., Sang, A. E., Hulbert, K., Sebag-Montefiore, L., Watkins, H., Clarke, K., Isbrandt, D., Wallis, J., & Neubauer, S. (2005). Reduced inotropic reserve and increased susceptibility to cardiac ischemia/reperfusion injury in phosphocreatine-deficient guanidinoacetate-N-methyltransferase-knockout mice. CIRCULATION, 111(19), 2477-2485. [19]. http://www.ncbi.nlm.nih.gov/pubmed/15883212?dopt=Citation

Vancouver

Michiel TH, Lygate CA, Fischer A, Schneider JE, Sang AE, Hulbert K et al. Reduced inotropic reserve and increased susceptibility to cardiac ischemia/reperfusion injury in phosphocreatine-deficient guanidinoacetate-N-methyltransferase-knockout mice. CIRCULATION. 2005;111(19):2477-2485. 19.

Bibtex

@article{c10c6cd8167a4fdd9f0a1e90e650cbc0,
title = "Reduced inotropic reserve and increased susceptibility to cardiac ischemia/reperfusion injury in phosphocreatine-deficient guanidinoacetate-N-methyltransferase-knockout mice.",
abstract = "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 (WT) and GAMT-/- mice. METHODS AND RESULTS: GAMT-/- mice did not show cardiac hypertrophy (myocyte cross-sectional areas, hypertrophy markers atrial natriuretic factor and beta-myosin heavy chain). Systolic and diastolic function, measured invasively (left ventricular conductance catheter) and noninvasively (MRI), were similar for WT and GAMT-/- mice. However, during inotropic stimulation with dobutamine, preload-recruitable stroke work failed to reach maximal levels of performance in GAMT-/- hearts (101+/-8 mm Hg in WT versus 59+/-7 mm Hg in GAMT-/-; P",
author = "Michiel, {Ten Hove} and Lygate, {Craig A} and Alexandra Fischer and Schneider, {J{\"u}rgen E} and Sang, {A Elisabeth} and Karen Hulbert and Liam Sebag-Montefiore and Hugh Watkins and Kieran Clarke and Dirk Isbrandt and Julie Wallis and Stefan Neubauer",
year = "2005",
language = "Deutsch",
volume = "111",
pages = "2477--2485",
journal = "CIRCULATION",
issn = "0009-7322",
publisher = "Lippincott Williams and Wilkins",
number = "19",

}

RIS

TY - JOUR

T1 - Reduced inotropic reserve and increased susceptibility to cardiac ischemia/reperfusion injury in phosphocreatine-deficient guanidinoacetate-N-methyltransferase-knockout mice.

AU - Michiel, Ten Hove

AU - Lygate, Craig A

AU - Fischer, Alexandra

AU - Schneider, Jürgen E

AU - Sang, A Elisabeth

AU - Hulbert, Karen

AU - Sebag-Montefiore, Liam

AU - Watkins, Hugh

AU - Clarke, Kieran

AU - Isbrandt, Dirk

AU - Wallis, Julie

AU - Neubauer, Stefan

PY - 2005

Y1 - 2005

N2 - 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 (WT) and GAMT-/- mice. METHODS AND RESULTS: GAMT-/- mice did not show cardiac hypertrophy (myocyte cross-sectional areas, hypertrophy markers atrial natriuretic factor and beta-myosin heavy chain). Systolic and diastolic function, measured invasively (left ventricular conductance catheter) and noninvasively (MRI), were similar for WT and GAMT-/- mice. However, during inotropic stimulation with dobutamine, preload-recruitable stroke work failed to reach maximal levels of performance in GAMT-/- hearts (101+/-8 mm Hg in WT versus 59+/-7 mm Hg in GAMT-/-; P

AB - 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 (WT) and GAMT-/- mice. METHODS AND RESULTS: GAMT-/- mice did not show cardiac hypertrophy (myocyte cross-sectional areas, hypertrophy markers atrial natriuretic factor and beta-myosin heavy chain). Systolic and diastolic function, measured invasively (left ventricular conductance catheter) and noninvasively (MRI), were similar for WT and GAMT-/- mice. However, during inotropic stimulation with dobutamine, preload-recruitable stroke work failed to reach maximal levels of performance in GAMT-/- hearts (101+/-8 mm Hg in WT versus 59+/-7 mm Hg in GAMT-/-; P

M3 - SCORING: Zeitschriftenaufsatz

VL - 111

SP - 2477

EP - 2485

JO - CIRCULATION

JF - CIRCULATION

SN - 0009-7322

IS - 19

M1 - 19

ER -