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1 Department of Transplant Surgery, D. Swarovski Research Laboratory, University Hospital Innsbruck, Innsbruck, Austria; Department of Transplant Surgery, D. Swarovski Research Laboratory, University Hospital Innsbruck, Innsbruck, Austria
2 Department of Transplant Surgery, D. Swarovski Research Laboratory, University Hospital Innsbruck, Innsbruck, Austria
3 Laboratory of Bioenergetics, Joseph Fourier University, Innsbruck, Austria
4 TIMC Laboratory, UMR5525 CNRS, Institute Albert Bonniot, Innsbruck, Austria
* To whom correspondence should be addressed. E-mail: andrei.kuznetsov{at}uibk.ac.at.
Mitochondria play a critical role in myocardial cold ischemia-reperfusion (CIR) and induction of apoptosis. The nature and extent of mitochondrial defects and cytochrome c (Cyt c) release were determined by high-resolution respirometry in permeabilized myocardial fibers. CIR in a rat heart transplant model resulted in variable contractile performance, correlating with the decline of ADP-stimulated respiration. Respiration with succinate or TMPD (substrates for complexes II and IV) was partially restored by added Cyt c, indicating Cyt c release. In contrast, NADH-linked respiration (glutamate+malate) was not stimulated by Cyt c, owing to a specific defect of complex I. CIR but not cold ischemia alone resulted in the loss of NADH-linked respiratory capacity, uncoupling of oxidative phosphorylation and Cyt c release. Mitochondria depleted of Cyt c by controlled hypo-osmotic shock provided a kinetic model of homogenous Cyt c depletion. Comparison to Cyt c control of respiration in CIR injured myocardial fibers indicated heterogeneity of Cyt c release. The complex I defect and uncoupling correlated with heterogeneous cytochrome c release, the extent of which increased with loss of cardiac performance. These results demonstrate a complex pattern of multiple mitochondrial damage as determinants of CIR injury of the heart.
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