Severe energy deprivation of human hibernating myocardium as possible common pathomechanism of contractile dysfunction, structural degeneration and cell death
Albrecht Elsässer, MD* ,*,
Klaus-Detlev Müller, MD ,
Woitek Skwara, MD,
Christoph Bode, MD*,
Wolfgang Kübler, MD, FRCP and
Achim M. Vogt, MD
* Department of Cardiology, University of Freiburg, Freiburg, Germany
Department of Experimental Cardiology, Max-Planck-Institute for Physiological and Clinical Research (W. G. Kerckhoff-Institute), Bad Nauheim, Germany
Kerckhoff-Clinic, Bad Nauheim, Germany
Department of Cardiology, University of Heidelberg, Heidelberg, Germany
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Figure 1 Myocardial contents. Myocardial metabolite contents for the cellular myocardial fraction (CMF) reflecting myocellular content are given as µmol/g wet weight. ATP = adenosine triphosphate; CP = creatine phosphate; Cr = creatine; ADP = adenosine diphosphate; AMP = adenosine monophosphate; Pi = inorganic phosphate. Open bars: controls; black bars: hibernating myocardium. Given are mean values ± SEM. *Significant differences (p values, see Table 2), n.s. = not significant.
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Figure 2 Energetic parameters related to contractile dysfunction (a) and tissue degeneration (b). Values for energy charge (EC), free energy of adenosine triphosphate (ATP) hydrolysis ( GATP) and estimated pH (a) as well as myocardial fibrosis and the adenosine diphosphate (ADP)/ATP ratio (b) in control (open bars) and hibernating myocardium (black bars), given as mean ± SEM. *Significant differences (analysis of variance, p values, see Table 2).
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