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Am J Physiol Heart Circ Physiol 282: H726-H733, 2002; doi:10.1152/ajpheart.00308.2001
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Vol. 282, Issue 2, H726-H733, February 2002

Cardiac dysfunction in mice lacking cytochrome-c oxidase subunit VIaH

Nina B. Radford1, Bang Wan2, Angela Richman2, Lidia S. Szczepaniak2, Jia-Ling Li2, Kang Li2, Kathy Pfeiffer3, Hermann Schägger3, Daniel J. Garry2,4, and Randall W. Moreadith5

1 The Cooper Clinic, Dallas 75230; 2 Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, Texas 75390; 3 Biochemie I, Zentrum der Biologischen Chemie, Universitäts-Klinikum, 60590 Frankfurt, Germany; 4 Molecular Biology Department, The University of Texas Southwestern Medical Center, Dallas, Texas 75390 - 8573; 5 ThromboGene, Chapel Hill, North Carolina 27514

Cytochrome-c oxidase subunit VIaH (COXVIaH) has been implicated in the modulation of COX activity. A gene-targeting strategy was undertaken to generate mice that lacked COXVIaH to determine its role in regulation of oxidative energy production and mechanical performance in cardiac muscle. Total COX activity was decreased in hearts from mutant mice, which appears to be a consequence of altered assembly of the holoenzyme COX. However, total myocardial ATP was not significantly different in wild-type and mutant mice. Myocardial performance was examined using the isolated working heart preparation. As left atrial filling pressure increased, hearts from mutant mice were unable to generate equivalent stroke work compared with hearts from wild-type mice. Direct measurement of left ventricular end-diastolic volume using magnetic resonance imaging revealed that cardiac dysfunction was a consequence of impaired ventricular filling or diastolic dysfunction. These findings suggest that a genetic deficiency of COXVIaH has a measurable impact on myocardial diastolic performance despite the presence of normal cellular ATP levels.

transgenic animals; diastolic dysfunction; energy metabolism; nuclear magnetic resonance spectroscopy


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