Difference between revisions of "Kuznetsov 2004 Am J Physiol Heart Circ Physiol"
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|title=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:H1633–41. | |title=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:H1633–41. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/14693685 PMID: 14693685 Open Access] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/14693685 PMID: 14693685 Open Access] | ||
|authors=Kuznetsov AV, Schneeberger S, Seiler R, Brandacher G, Mark W, Steurer W, Saks V, Usson Y, Margreiter R, Gnaiger | |authors=Kuznetsov AV, Schneeberger S, Seiler R, Brandacher G, Mark W, Steurer W, Saks V, Usson Y, Margreiter R, Gnaiger Erich | ||
|year=2004 | |year=2004 | ||
|journal=Am J Physiol Heart Circ Physiol | |journal=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. | |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. | ||
|keywords=Heart preservation, Complex I injury, Permeabilized myocardial fibers | |keywords=Heart preservation, Complex I injury, Permeabilized myocardial fibers | ||
|mipnetlab=AT Innsbruck Gnaiger E, EE Tallinn Saks VA, FR Grenoble Saks VA, AT Innsbruck | |mipnetlab=AT Innsbruck Gnaiger E, EE Tallinn Saks VA, FR Grenoble Saks VA, AT Innsbruck Oroboros, EE Tallinn Kaambre T | ||
}} | }} | ||
::::* [[Tissue storage]] | |||
== Cited by == | |||
::* 55 articles in PubMed (2021-12-27) https://pubmed.ncbi.nlm.nih.gov/14693685/ | |||
{{Template:Cited by Gnaiger 2020 BEC MitoPathways}} | |||
{{Labeling | {{Labeling | ||
|area=Respiration, mt-Biogenesis;mt-density, mt-Medicine | |area=Respiration, mt-Biogenesis;mt-density, mt-Medicine | ||
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|pathways=N, S, CIV, ROX | |pathways=N, S, CIV, ROX | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
| | |additional=BEC 2020.2 | ||
}} | }} | ||
Latest revision as of 14:01, 27 December 2021
| 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:H1633–41. |
Kuznetsov AV, Schneeberger S, Seiler R, Brandacher G, Mark W, Steurer W, Saks V, Usson Y, Margreiter R, Gnaiger Erich (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. • Keywords: Heart preservation, Complex I injury, Permeabilized myocardial fibers
• O2k-Network Lab: AT Innsbruck Gnaiger E, EE Tallinn Saks VA, FR Grenoble Saks VA, AT Innsbruck Oroboros, EE Tallinn Kaambre T
Cited by
- 55 articles in PubMed (2021-12-27) https://pubmed.ncbi.nlm.nih.gov/14693685/
- Gnaiger E (2020) Mitochondrial pathways and respiratory control. An introduction to OXPHOS analysis. 5th ed. Bioenerg Commun 2020.2. https://doi.org/10.26124/bec:2020-0002
Labels: MiParea: Respiration, mt-Biogenesis;mt-density, mt-Medicine
Stress:Ischemia-reperfusion Organism: Rat Tissue;cell: Heart Preparation: Intact organ, Permeabilized tissue, SMP, Enzyme Enzyme: Marker enzyme Regulation: Coupling efficiency;uncoupling, Cyt c, Flux control, Threshold;excess capacity Coupling state: LEAK, OXPHOS Pathway: N, S, CIV, ROX HRR: Oxygraph-2k
BEC 2020.2
