Kuznetsov 2004 Am J Physiol Heart Circ Physiol

From Bioblast
Revision as of 16:47, 8 October 2010 by Biljana (talk | contribs)
Publications in the MiPMap
Kuznetsov AV, Schneeberger S, Seiler R, Brandacher G, Mark W, Steurer W, Saks V, Usson Y, Margreiter R, Gnaiger E (2004) Mitochondrial defects and heterogeneous cytochrome c release after cardiac cold ischemia and reperfusion. Am. J. Physiol. Heart Circ. Physiol. 286: H1633–H1641.

Β» [[Has info::PMID: 14693685]]

Kuznetsov AV, Schneeberger S, Seiler R, Brandacher G, Mark W, Steurer W, Saks V, Usson Y, Margreiter R, Gnaiger E (2004) Am. J. Physiol. Heart Circ. Physiol.

Abstract: 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 N,N,N',N'-tetramethyl-p-phenylenediamine dihydrochloride (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 hypoosmotic 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 Cyt 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. β€’ Keywords: Respiration, Heart preservation, Complex I injury, Permeabilized myocardial fibers

β€’ O2k-Network Lab: AT_Innsbruck_GnaigerE


Labels:

Stress:Ischemia-Reperfusion; Preservation  Organism: Rat  Tissue;cell: Cardiac Muscle  Preparation: Intact Organ, Permeabilized Cell or Tissue; Homogenate, Oxidase; Biochemical Oxidation, Enzyme 

Regulation: Respiration; OXPHOS; ETS Capacity, Coupling; Membrane Potential, Mitochondrial Biogenesis; Mitochondrial Density, Substrate; Glucose; TCA Cycle 


HRR: Oxygraph-2k 


Cookies help us deliver our services. By using our services, you agree to our use of cookies.