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Mitochondrial defects and heterogeneous cytochrome c release after cardiac cold ischemia and reperfusion
1 Department of Transplant Surgery, D. Swarovski Research Laboratory, University Hospital Innsbruck, A-6020 Innsbruck, Austria; 2 Laboratory of Bioenergetics, Joseph Fourier University, Grenoble Cedex 9; and 3 Techniques de l'Imagerie de la Modelisation et de la Cognition Laboratory, UMR5525 Ce...
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| Published in: | American journal of physiology. Heart and circulatory physiology 2004-05, Vol.286 (5), p.H1633-H1641 |
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| container_end_page | H1641 |
| container_issue | 5 |
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| container_title | American journal of physiology. Heart and circulatory physiology |
| container_volume | 286 |
| creator | Kuznetsov, Andrey V Schneeberger, Stefan Seiler, Rudiger Brandacher, Gerald Mark, Walter Steurer, Wolfgang Saks, Valdur Usson, Yves Margreiter, Raimund Gnaiger, Erich |
| description | 1 Department of Transplant Surgery, D. Swarovski Research Laboratory, University Hospital Innsbruck, A-6020 Innsbruck, Austria; 2 Laboratory of Bioenergetics, Joseph Fourier University, Grenoble Cedex 9; and 3 Techniques de l'Imagerie de la Modelisation et de la Cognition Laboratory, UMR5525 Centre National de la Recherche Scientifique, Institute Albert Bonniot, Grenoble 38706, France
Submitted 21 July 2003
; accepted in final form 19 December 2003
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.
respiration; heart preservation; complex I injury; permeabilized myocardial fibers
Address for reprint requests and other correspondence: E. Gnaiger, Dept. of Transplant Surgery, D. Swarovski Research Laboratory, Univ. Hospital Innsbruck, Innrain 66/6, A-6020 Innsbruck, Austria (E-mail: erich.gnaiger{at}uibk.ac.at ). |
| doi_str_mv | 10.1152/ajpheart.00701.2003 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_highw</sourceid><recordid>TN_cdi_highwire_physiology_ajpheart_286_5_H1633</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>71807964</sourcerecordid><originalsourceid>FETCH-LOGICAL-c429t-137548cbd5a3569f4278bfb8df0e554f2c609a4eddbadb359c1b0fa5194c1dab3</originalsourceid><addsrcrecordid>eNp1kUFv0zAYhi0EYmXwC5CQT0g7pLPj2InFaZoYRSriMs6WY39uPDl1sBOg_35JWzYunCzZz_vo8_ci9J6SNaW8vNYPQwc6jWtCakLXJSHsBVrNL2VBOZMv0YowwQpBGb9Ab3J-IITwWrDX6IJWQjLR8BXqvvkxmi7ubfI6YAsOzJix3lvcwQgp7mAPccrYHBYuxR6wwQkC6AxYuxnBRifrtcEmBot9Nh30Xh8VCQZIbso-7t-iV06HDO_O5yX6cff5_nZTbL9_-Xp7sy1MVcqxoKzmVWNayzXjQrqqrJvWtY11BDivXGkEkboCa1ttW8aloS1xmlNZGWp1yy7R1cnb6aCG5HudDipqrzY3W7XcEUJlyWn9i87sxxM7pPhzgjyqfh4fQtDHP6uaNqSWoppBdgJNijkncE9mStRShvpbhjqWoZYy5tSHs35qe7DPmfP2Z-D6PKvfdb99AjV0h3lZIe4Oz8ayEYqrDRVsUX76f-JuCuEe_oxP0X-SarCOPQI8rK_W</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>71807964</pqid></control><display><type>article</type><title>Mitochondrial defects and heterogeneous cytochrome c release after cardiac cold ischemia and reperfusion</title><source>American Physiological Society Free</source><creator>Kuznetsov, Andrey V ; Schneeberger, Stefan ; Seiler, Rudiger ; Brandacher, Gerald ; Mark, Walter ; Steurer, Wolfgang ; Saks, Valdur ; Usson, Yves ; Margreiter, Raimund ; Gnaiger, Erich</creator><creatorcontrib>Kuznetsov, Andrey V ; Schneeberger, Stefan ; Seiler, Rudiger ; Brandacher, Gerald ; Mark, Walter ; Steurer, Wolfgang ; Saks, Valdur ; Usson, Yves ; Margreiter, Raimund ; Gnaiger, Erich</creatorcontrib><description>1 Department of Transplant Surgery, D. Swarovski Research Laboratory, University Hospital Innsbruck, A-6020 Innsbruck, Austria; 2 Laboratory of Bioenergetics, Joseph Fourier University, Grenoble Cedex 9; and 3 Techniques de l'Imagerie de la Modelisation et de la Cognition Laboratory, UMR5525 Centre National de la Recherche Scientifique, Institute Albert Bonniot, Grenoble 38706, France
Submitted 21 July 2003
; accepted in final form 19 December 2003
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.
respiration; heart preservation; complex I injury; permeabilized myocardial fibers
Address for reprint requests and other correspondence: E. Gnaiger, Dept. of Transplant Surgery, D. Swarovski Research Laboratory, Univ. Hospital Innsbruck, Innrain 66/6, A-6020 Innsbruck, Austria (E-mail: erich.gnaiger{at}uibk.ac.at ).</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.00701.2003</identifier><identifier>PMID: 14693685</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Animals ; Bioengineering ; Cryopreservation ; Cytochromes c ; Cytochromes c - metabolism ; Electron Transport Complex I ; Electron Transport Complex I - metabolism ; Heart ; Heart - physiopathology ; Imaging ; In Vitro Techniques ; Kinetics ; Life Sciences ; Male ; Mitochondria, Heart ; Mitochondria, Heart - metabolism ; Myocardial Contraction ; Myocardial Ischemia ; Myocardial Ischemia - metabolism ; Myocardial Ischemia - physiopathology ; Myocardial Reperfusion Injury ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - physiopathology ; Oxygen Consumption ; Rats ; Rats, Inbred Lew</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2004-05, Vol.286 (5), p.H1633-H1641</ispartof><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c429t-137548cbd5a3569f4278bfb8df0e554f2c609a4eddbadb359c1b0fa5194c1dab3</citedby><cites>FETCH-LOGICAL-c429t-137548cbd5a3569f4278bfb8df0e554f2c609a4eddbadb359c1b0fa5194c1dab3</cites><orcidid>0000-0003-0242-191X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,786,790,891,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14693685$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00192517$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Kuznetsov, Andrey V</creatorcontrib><creatorcontrib>Schneeberger, Stefan</creatorcontrib><creatorcontrib>Seiler, Rudiger</creatorcontrib><creatorcontrib>Brandacher, Gerald</creatorcontrib><creatorcontrib>Mark, Walter</creatorcontrib><creatorcontrib>Steurer, Wolfgang</creatorcontrib><creatorcontrib>Saks, Valdur</creatorcontrib><creatorcontrib>Usson, Yves</creatorcontrib><creatorcontrib>Margreiter, Raimund</creatorcontrib><creatorcontrib>Gnaiger, Erich</creatorcontrib><title>Mitochondrial defects and heterogeneous cytochrome c release after cardiac cold ischemia and reperfusion</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>1 Department of Transplant Surgery, D. Swarovski Research Laboratory, University Hospital Innsbruck, A-6020 Innsbruck, Austria; 2 Laboratory of Bioenergetics, Joseph Fourier University, Grenoble Cedex 9; and 3 Techniques de l'Imagerie de la Modelisation et de la Cognition Laboratory, UMR5525 Centre National de la Recherche Scientifique, Institute Albert Bonniot, Grenoble 38706, France
Submitted 21 July 2003
; accepted in final form 19 December 2003
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.
respiration; heart preservation; complex I injury; permeabilized myocardial fibers
Address for reprint requests and other correspondence: E. Gnaiger, Dept. of Transplant Surgery, D. Swarovski Research Laboratory, Univ. Hospital Innsbruck, Innrain 66/6, A-6020 Innsbruck, Austria (E-mail: erich.gnaiger{at}uibk.ac.at ).</description><subject>Animals</subject><subject>Bioengineering</subject><subject>Cryopreservation</subject><subject>Cytochromes c</subject><subject>Cytochromes c - metabolism</subject><subject>Electron Transport Complex I</subject><subject>Electron Transport Complex I - metabolism</subject><subject>Heart</subject><subject>Heart - physiopathology</subject><subject>Imaging</subject><subject>In Vitro Techniques</subject><subject>Kinetics</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Mitochondria, Heart</subject><subject>Mitochondria, Heart - metabolism</subject><subject>Myocardial Contraction</subject><subject>Myocardial Ischemia</subject><subject>Myocardial Ischemia - metabolism</subject><subject>Myocardial Ischemia - physiopathology</subject><subject>Myocardial Reperfusion Injury</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - physiopathology</subject><subject>Oxygen Consumption</subject><subject>Rats</subject><subject>Rats, Inbred Lew</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNp1kUFv0zAYhi0EYmXwC5CQT0g7pLPj2InFaZoYRSriMs6WY39uPDl1sBOg_35JWzYunCzZz_vo8_ci9J6SNaW8vNYPQwc6jWtCakLXJSHsBVrNL2VBOZMv0YowwQpBGb9Ab3J-IITwWrDX6IJWQjLR8BXqvvkxmi7ubfI6YAsOzJix3lvcwQgp7mAPccrYHBYuxR6wwQkC6AxYuxnBRifrtcEmBot9Nh30Xh8VCQZIbso-7t-iV06HDO_O5yX6cff5_nZTbL9_-Xp7sy1MVcqxoKzmVWNayzXjQrqqrJvWtY11BDivXGkEkboCa1ttW8aloS1xmlNZGWp1yy7R1cnb6aCG5HudDipqrzY3W7XcEUJlyWn9i87sxxM7pPhzgjyqfh4fQtDHP6uaNqSWoppBdgJNijkncE9mStRShvpbhjqWoZYy5tSHs35qe7DPmfP2Z-D6PKvfdb99AjV0h3lZIe4Oz8ayEYqrDRVsUX76f-JuCuEe_oxP0X-SarCOPQI8rK_W</recordid><startdate>20040501</startdate><enddate>20040501</enddate><creator>Kuznetsov, Andrey V</creator><creator>Schneeberger, Stefan</creator><creator>Seiler, Rudiger</creator><creator>Brandacher, Gerald</creator><creator>Mark, Walter</creator><creator>Steurer, Wolfgang</creator><creator>Saks, Valdur</creator><creator>Usson, Yves</creator><creator>Margreiter, Raimund</creator><creator>Gnaiger, Erich</creator><general>American Physiological Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0003-0242-191X</orcidid></search><sort><creationdate>20040501</creationdate><title>Mitochondrial defects and heterogeneous cytochrome c release after cardiac cold ischemia and reperfusion</title><author>Kuznetsov, Andrey V ; Schneeberger, Stefan ; Seiler, Rudiger ; Brandacher, Gerald ; Mark, Walter ; Steurer, Wolfgang ; Saks, Valdur ; Usson, Yves ; Margreiter, Raimund ; Gnaiger, Erich</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c429t-137548cbd5a3569f4278bfb8df0e554f2c609a4eddbadb359c1b0fa5194c1dab3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Bioengineering</topic><topic>Cryopreservation</topic><topic>Cytochromes c</topic><topic>Cytochromes c - metabolism</topic><topic>Electron Transport Complex I</topic><topic>Electron Transport Complex I - metabolism</topic><topic>Heart</topic><topic>Heart - physiopathology</topic><topic>Imaging</topic><topic>In Vitro Techniques</topic><topic>Kinetics</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Mitochondria, Heart</topic><topic>Mitochondria, Heart - metabolism</topic><topic>Myocardial Contraction</topic><topic>Myocardial Ischemia</topic><topic>Myocardial Ischemia - metabolism</topic><topic>Myocardial Ischemia - physiopathology</topic><topic>Myocardial Reperfusion Injury</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - physiopathology</topic><topic>Oxygen Consumption</topic><topic>Rats</topic><topic>Rats, Inbred Lew</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kuznetsov, Andrey V</creatorcontrib><creatorcontrib>Schneeberger, Stefan</creatorcontrib><creatorcontrib>Seiler, Rudiger</creatorcontrib><creatorcontrib>Brandacher, Gerald</creatorcontrib><creatorcontrib>Mark, Walter</creatorcontrib><creatorcontrib>Steurer, Wolfgang</creatorcontrib><creatorcontrib>Saks, Valdur</creatorcontrib><creatorcontrib>Usson, Yves</creatorcontrib><creatorcontrib>Margreiter, Raimund</creatorcontrib><creatorcontrib>Gnaiger, Erich</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kuznetsov, Andrey V</au><au>Schneeberger, Stefan</au><au>Seiler, Rudiger</au><au>Brandacher, Gerald</au><au>Mark, Walter</au><au>Steurer, Wolfgang</au><au>Saks, Valdur</au><au>Usson, Yves</au><au>Margreiter, Raimund</au><au>Gnaiger, Erich</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mitochondrial defects and heterogeneous cytochrome c release after cardiac cold ischemia and reperfusion</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2004-05-01</date><risdate>2004</risdate><volume>286</volume><issue>5</issue><spage>H1633</spage><epage>H1641</epage><pages>H1633-H1641</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>1 Department of Transplant Surgery, D. Swarovski Research Laboratory, University Hospital Innsbruck, A-6020 Innsbruck, Austria; 2 Laboratory of Bioenergetics, Joseph Fourier University, Grenoble Cedex 9; and 3 Techniques de l'Imagerie de la Modelisation et de la Cognition Laboratory, UMR5525 Centre National de la Recherche Scientifique, Institute Albert Bonniot, Grenoble 38706, France
Submitted 21 July 2003
; accepted in final form 19 December 2003
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.
respiration; heart preservation; complex I injury; permeabilized myocardial fibers
Address for reprint requests and other correspondence: E. Gnaiger, Dept. of Transplant Surgery, D. Swarovski Research Laboratory, Univ. Hospital Innsbruck, Innrain 66/6, A-6020 Innsbruck, Austria (E-mail: erich.gnaiger{at}uibk.ac.at ).</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>14693685</pmid><doi>10.1152/ajpheart.00701.2003</doi><orcidid>https://orcid.org/0000-0003-0242-191X</orcidid></addata></record> |
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| ispartof | American journal of physiology. Heart and circulatory physiology, 2004-05, Vol.286 (5), p.H1633-H1641 |
| issn | 0363-6135 1522-1539 |
| language | eng |
| recordid | cdi_highwire_physiology_ajpheart_286_5_H1633 |
| source | American Physiological Society Free |
| subjects | Animals Bioengineering Cryopreservation Cytochromes c Cytochromes c - metabolism Electron Transport Complex I Electron Transport Complex I - metabolism Heart Heart - physiopathology Imaging In Vitro Techniques Kinetics Life Sciences Male Mitochondria, Heart Mitochondria, Heart - metabolism Myocardial Contraction Myocardial Ischemia Myocardial Ischemia - metabolism Myocardial Ischemia - physiopathology Myocardial Reperfusion Injury Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - physiopathology Oxygen Consumption Rats Rats, Inbred Lew |
| title | Mitochondrial defects and heterogeneous cytochrome c release after cardiac cold ischemia and reperfusion |
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