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Am J Physiol Heart Circ Physiol 280: H2623-H2630, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 6, H2623-H2630, June 2001

Maintained contractile reserve in a transgenic mouse model of myocardial stunning

Harald Kögler1,3,4, David G. Soergel2,3, Anne M. Murphy2,3, and Eduardo Marbán1,3

1 Departments of Medicine and 2 Pediatrics and 3 Institute of Molecular Cardiobiology, Johns Hopkins University, Baltimore, Maryland 21205; and 4 Department of Cardiology and Pneumology, Georg-August-University, 37075 Göttingen, Germany

Cardiac excitation-contraction (E-C) coupling is impaired at the myofilament level in the reversible postischemic dysfunction known as "stunned" myocardium. We characterized tension development and calcium cycling in intact isolated trabeculae from transgenic (TG) mice expressing the major proteolytic degradation fragment of troponin I (TnI) found in stunned myocardium (TnI1-193) and determined the ATPase activity of myofibrils extracted from TG and non-TG mouse hearts. The phenotype of these mice at baseline recapitulates that of stunning. Here, we address the question of whether contractile reserve is preserved in these mice, as it is in genuine stunned myocardium. During twitch contractions, calcium cycling was normal, whereas tension was greatly reduced, compared with non-TG controls. A decrease in maximum Ca2+-activated tension and Ca2+ desensitization of the myofilaments accounted for this contractile dysfunction. The decrease in maximum tension was paralleled by an equivalent decrease in maximum Ca2+-activated myofibrillar ATPase activity. Exposure to high calcium or isoproterenol recruited a sizable contractile reserve in TG muscles, which was proportionately similar to that in control muscles but scaled downward in amplitude. These results suggest that calcium regulatory pathways and beta -adrenergic signal transduction remain intact in isolated trabeculae from stunned TG mice, further recapitulating key features of genuine stunned myocardium.

cardiac excitation-contraction coupling; signal transduction; calcium ion sensitivity


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