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Am J Physiol Heart Circ Physiol 277: H308-H317, 1999;
0363-6135/99 $5.00
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Vol. 277, Issue 1, H308-H317, July 1999

Cardiac performance and creatine kinase flux during inhibition of ATP synthesis in the perfused rat heart

P. Mateo1, V. Stepanov1, B. Gillet2, J.-C. Beloeil2, and J. A. Hoerter1

1 Unité 446, Institut National de la Santé et de la Recherche Médicale, Cardiologie Cellulaire et Moléculaire, Université Paris-Sud, 92296 Chatenay Malabry; and 2 Résonance Magnétique Nucléaire Biologique, Institut de Chimie des Substances Naturelles, Centre National de la Recherche Scientifique, 91198 Gif sur Yvette, France

To study the relation among mitochondrial energy supply, cardiac performance, and energy transfer through creatine kinase (CK), two acute models of inhibition of ATP synthesis were compared in the isovolumic acetate-perfused rat heart. Similar impairments of mechanical performance (rate-pressure product, RPP) were achieved by various stepwise decreases in O2 supply (PO2 down to 20% of control) or by infusing CN (0.15-0.25 mM). The forward CK flux measured by saturation-transfer 31P NMR spectroscopy was 6.1 ± 0.4 mM/s in control hearts. Only after severe hypoxia (PO2 < 40% of control) did CK flux drop (to 1.9 ± 0.2 mM/s at PO2 = 25% of control) together with impaired systolic activity and a rise in end-diastolic pressure. In contrast, in mild hypoxia CK flux remained constant and similar to control (5.3 ± 0.5 mM/s, not significant) despite a twofold reduction in systolic activity. Similarly in all CN groups, constant CK flux was maintained for a threefold reduction in RPP, showing the absence of a relation between cardiac performance and global NMR-measured CK flux during mild ATP synthesis inhibition.

creatine phosphate shuttle; oxidative phosphorylation inhibition and energetics; oxygen consumption; creatine kinase kinetics; rigor; magnetization transfer; work


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