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Am J Physiol Heart Circ Physiol 282: H349-H356, 2002; doi:10.1152/ajpheart.00024.2001
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Vol. 282, Issue 1, H349-H356, January 2002

Load-dependent induction of apoptosis in multicellular myocardial preparations

P. M. L. Janssen1, G. Hasenfuss1, O. Zeitz1, S. E. Lehnart1, J. Prestle1, D. Darmer2, J. Holtz2, and H. Schumann3

1 Abteilung Kardiologie und Pneumologie, Universität Göttingen, Göttingen D-37075; and 2 Institut für Pathophysiologie and 3 Zentrale Arbeitsgruppe der Medizinische Fakultät, Universität Halle-Wittenberg, Halle 06108, Germany

10.1152/ajpheart.00024.2001.---Increased mechanical load has been proposed as an inductor of apoptosis, but it is unknown whether this can occur in the range of pre- and afterloads that prevail in the beating heart. We investigated apoptosis in cultured rabbit multicellular myocardial preparations over several days. Muscles contracted in absence of pre- and afterload (unloaded isotonic), in absence of preload but in presence of afterload (unloaded isometric), or in presence of both (loaded isometric). After up to 48 h of continuous contractions, apoptosis was assessed by TdT-mediated nick-end labeling (TUNEL) assay and DNA ladder analysis. In muscles that contracted loaded isometric, apoptosis was detected after 6-24 h. After 48 h, apoptosis was most prominent in this group, reflected by a high level of DNA ladder intensity (DLI; 27.8 ± 11.5), whereas Bcl-xL (on RNA level) was significantly downregulated, and Fas remained unchanged. In unloaded isometric preparations, apoptosis was significantly less (6.9 ± 5.9 DLI) and very similar to those contracting unloaded isotonic (6.1 ± 5.1 DLI). We conclude that load-dependent apoptosis can occur at sarcomere lengths achievable in vivo and may mainly result from increased preload.

preload; afterload; calcium; trabeculae; stretch; myocyte; Bcl-xL; Fas; TdT-mediated nick-end labeling


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