Impaired mitochondrial function in chronically ischemic human heart
Chronic ischemic heart disease is associated with myocardial hypoperfusion. The resulting hypoxia potentially inflicts damage upon the mitochondria, leading to a compromised energetic state. Furthermore, ischemic damage may cause excessive production of reactive oxygen species (ROS), producing mitoc...
Saved in:
| Published in | American journal of physiology. Heart and circulatory physiology Vol. 304; no. 11; pp. H1407 - H1414 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Physiological Society
01.06.2013
|
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | Chronic ischemic heart disease is associated with myocardial hypoperfusion. The resulting hypoxia potentially inflicts damage upon the mitochondria, leading to a compromised energetic state. Furthermore, ischemic damage may cause excessive production of reactive oxygen species (ROS), producing mitochondrial damage, hereby reinforcing a vicious circle. Ischemic preconditioning has been proven protective in acute ischemia, but the subject of chronic ischemic preconditioning has not been explored in humans. We hypothesized that mitochondrial respiratory capacity would be diminished in chronic ischemic regions of human myocardium but that these mitochondria would be more resistant to ex vivo ischemia and, second, that ROS generation would be higher in ischemic myocardium. The aim of this study was to test mitochondrial respiratory capacity during hyperoxia and hypoxia, to investigate ROS production, and finally to assess myocardial antioxidant levels. Mitochondrial respiration in biopsies from ischemic and nonischemic regions from the left ventricle of the same heart was compared in nine human subjects. Maximal oxidative phosphorylation capacity in fresh muscle fibers was lower in ischemic compared with nonischemic myocardium ( P < 0.05), but the degree of coupling (respiratory control ratio) did not differ ( P > 0.05). The presence of ex vivo hypoxia did not reveal any chronic ischemic preconditioning of the ischemic myocardial regions ( P > 0.05). ROS production was higher in ischemic myocardium ( P < 0.05), and the levels of antioxidant protein expression was lower. Diminished mitochondrial respiration capacity and excessive ROS production demonstrate an impaired mitochondrial function in ischemic human heart muscle. No chronic ischemic preconditioning effect was found. |
|---|---|
| AbstractList | Chronic ischemic heart disease is associated with myocardial hypoperfusion. The resulting hypoxia potentially inflicts damage upon the mitochondria, leading to a compromised energetic state. Furthermore, ischemic damage may cause excessive production of reactive oxygen species (ROS), producing mitochondrial damage, hereby reinforcing a vicious circle. Ischemic preconditioning has been proven protective in acute ischemia, but the subject of chronic ischemic preconditioning has not been explored in humans. We hypothesized that mitochondrial respiratory capacity would be diminished in chronic ischemic regions of human myocardium but that these mitochondria would be more resistant to ex vivo ischemia and, second, that ROS generation would be higher in ischemic myocardium. The aim of this study was to test mitochondrial respiratory capacity during hyperoxia and hypoxia, to investigate ROS production, and finally to assess myocardial antioxidant levels. Mitochondrial respiration in biopsies from ischemic and nonischemic regions from the left ventricle of the same heart was compared in nine human subjects. Maximal oxidative phosphorylation capacity in fresh muscle fibers was lower in ischemic compared with nonischemic myocardium (P < 0.05), but the degree of coupling (respiratory control ratio) did not differ (P > 0.05). The presence of ex vivo hypoxia did not reveal any chronic ischemic preconditioning of the ischemic myocardial regions (P > 0.05). ROS production was higher in ischemic myocardium (P < 0.05), and the levels of antioxidant protein expression was lower. Diminished mitochondrial respiration capacity and excessive ROS production demonstrate an impaired mitochondrial function in ischemic human heart muscle. No chronic ischemic preconditioning effect was found.Chronic ischemic heart disease is associated with myocardial hypoperfusion. The resulting hypoxia potentially inflicts damage upon the mitochondria, leading to a compromised energetic state. Furthermore, ischemic damage may cause excessive production of reactive oxygen species (ROS), producing mitochondrial damage, hereby reinforcing a vicious circle. Ischemic preconditioning has been proven protective in acute ischemia, but the subject of chronic ischemic preconditioning has not been explored in humans. We hypothesized that mitochondrial respiratory capacity would be diminished in chronic ischemic regions of human myocardium but that these mitochondria would be more resistant to ex vivo ischemia and, second, that ROS generation would be higher in ischemic myocardium. The aim of this study was to test mitochondrial respiratory capacity during hyperoxia and hypoxia, to investigate ROS production, and finally to assess myocardial antioxidant levels. Mitochondrial respiration in biopsies from ischemic and nonischemic regions from the left ventricle of the same heart was compared in nine human subjects. Maximal oxidative phosphorylation capacity in fresh muscle fibers was lower in ischemic compared with nonischemic myocardium (P < 0.05), but the degree of coupling (respiratory control ratio) did not differ (P > 0.05). The presence of ex vivo hypoxia did not reveal any chronic ischemic preconditioning of the ischemic myocardial regions (P > 0.05). ROS production was higher in ischemic myocardium (P < 0.05), and the levels of antioxidant protein expression was lower. Diminished mitochondrial respiration capacity and excessive ROS production demonstrate an impaired mitochondrial function in ischemic human heart muscle. No chronic ischemic preconditioning effect was found. Chronic ischemic heart disease is associated with myocardial hypoperfusion. The resulting hypoxia potentially inflicts damage upon the mitochondria, leading to a compromised energetic state. Furthermore, ischemic damage may cause excessive production of reactive oxygen species (ROS), producing mitochondrial damage, hereby reinforcing a vicious circle. Ischemic preconditioning has been proven protective in acute ischemia, but the subject of chronic ischemic preconditioning has not been explored in humans. We hypothesized that mitochondrial respiratory capacity would be diminished in chronic ischemic regions of human myocardium but that these mitochondria would be more resistant to ex vivo ischemia and, second, that ROS generation would be higher in ischemic myocardium. The aim of this study was to test mitochondrial respiratory capacity during hyperoxia and hypoxia, to investigate ROS production, and finally to assess myocardial antioxidant levels. Mitochondrial respiration in biopsies from ischemic and nonischemic regions from the left ventricle of the same heart was compared in nine human subjects. Maximal oxidative phosphorylation capacity in fresh muscle fibers was lower in ischemic compared with nonischemic myocardium (P < 0.05), but the degree of coupling (respiratory control ratio) did not differ (P > 0.05). The presence of ex vivo hypoxia did not reveal any chronic ischemic preconditioning of the ischemic myocardial regions (P > 0.05). ROS production was higher in ischemic myocardium (P < 0.05), and the levels of antioxidant protein expression was lower. Diminished mitochondrial respiration capacity and excessive ROS production demonstrate an impaired mitochondrial function in ischemic human heart muscle. No chronic ischemic preconditioning effect was found. [PUBLICATION ABSTRACT] Chronic ischemic heart disease is associated with myocardial hypoperfusion. The resulting hypoxia potentially inflicts damage upon the mitochondria, leading to a compromised energetic state. Furthermore, ischemic damage may cause excessive production of reactive oxygen species (ROS), producing mitochondrial damage, hereby reinforcing a vicious circle. Ischemic preconditioning has been proven protective in acute ischemia, but the subject of chronic ischemic preconditioning has not been explored in humans. We hypothesized that mitochondrial respiratory capacity would be diminished in chronic ischemic regions of human myocardium but that these mitochondria would be more resistant to ex vivo ischemia and, second, that ROS generation would be higher in ischemic myocardium. The aim of this study was to test mitochondrial respiratory capacity during hyperoxia and hypoxia, to investigate ROS production, and finally to assess myocardial antioxidant levels. Mitochondrial respiration in biopsies from ischemic and nonischemic regions from the left ventricle of the same heart was compared in nine human subjects. Maximal oxidative phosphorylation capacity in fresh muscle fibers was lower in ischemic compared with nonischemic myocardium ( P < 0.05), but the degree of coupling (respiratory control ratio) did not differ ( P > 0.05). The presence of ex vivo hypoxia did not reveal any chronic ischemic preconditioning of the ischemic myocardial regions ( P > 0.05). ROS production was higher in ischemic myocardium ( P < 0.05), and the levels of antioxidant protein expression was lower. Diminished mitochondrial respiration capacity and excessive ROS production demonstrate an impaired mitochondrial function in ischemic human heart muscle. No chronic ischemic preconditioning effect was found. |
| Author | Hey-Mogensen, Martin Steinbrüchel, Daniel Larsen, Steen Dela, Flemming Stride, Nis Prats, Clara Køber, Lars Hansen, Christina N. |
| Author_xml | – sequence: 1 givenname: Nis surname: Stride fullname: Stride, Nis organization: Xlab, Center for Healthy Aging, Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 2 givenname: Steen surname: Larsen fullname: Larsen, Steen organization: Xlab, Center for Healthy Aging, Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 3 givenname: Martin surname: Hey-Mogensen fullname: Hey-Mogensen, Martin organization: Xlab, Center for Healthy Aging, Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 4 givenname: Christina N. surname: Hansen fullname: Hansen, Christina N. organization: Xlab, Center for Healthy Aging, Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 5 givenname: Clara surname: Prats fullname: Prats, Clara organization: Xlab, Center for Healthy Aging, Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 6 givenname: Daniel surname: Steinbrüchel fullname: Steinbrüchel, Daniel organization: Department of Cardiothoracic Surgery, University of Copenhagen, Copenhagen, Denmark; and – sequence: 7 givenname: Lars surname: Køber fullname: Køber, Lars organization: Department of Cardiology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark – sequence: 8 givenname: Flemming surname: Dela fullname: Dela, Flemming organization: Xlab, Center for Healthy Aging, Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23542918$$D View this record in MEDLINE/PubMed |
| BookMark | eNp9kTtrwzAUhUVJaR7tLygUQ5cuTvWwZGssoY9AoEs7C1mWsYItpZI95N9XzqNDhnKHO9zvXA7nzMHEOqsBuEdwiRDFz3K7a7T0_RJCztESQ4SvwCxecIoo4RMwg4SRlCFCp2AewhZCSHNGbsAUE5phjooZWK27nTReV0lneqcaZytvZJvUg1W9cTYxNlGNd9Yo2bb7xATV6M6opBk6aZODgVtwXcs26LvTXoDvt9ev1Ue6-Xxfr142qSKc92kpEeM1KmrIkc6YKqiqaFZjmktSsqpUOaKaVTqLDMMFLmpOFCqrnFRIYcLJAjwd_-68-xl06EUX7ei2lVa7IQhEGIVx2Ig-XqBbN3gb3R0onFNMWaQeTtRQdroSO2866ffiHE8EyBFQ3oXgdf2HICjGEsS5BHEoQYwlRBW_UCnTyzHN3kvT_qv9BT0ojlw |
| CODEN | AJPPDI |
| CitedBy_id | crossref_primary_10_1152_ajpheart_00797_2012 crossref_primary_10_1038_s41598_019_40419_7 crossref_primary_10_1253_circj_CJ_14_0728 crossref_primary_10_1016_j_athoracsur_2017_03_004 crossref_primary_10_1016_j_jacc_2015_09_010 crossref_primary_10_1016_j_yexcr_2016_10_021 crossref_primary_10_1093_cvr_cvad146 crossref_primary_10_1152_ajpheart_00945_2015 crossref_primary_10_1016_j_ijcard_2014_09_206 crossref_primary_10_1002_ehf2_13607 crossref_primary_10_1007_s12265_023_10382_w crossref_primary_10_1038_s41598_021_81797_1 crossref_primary_10_1152_ajpheart_00227_2014 crossref_primary_10_1016_j_peptides_2017_04_009 crossref_primary_10_1038_s12276_019_0214_6 crossref_primary_10_1161_CIRCHEARTFAILURE_113_000912 crossref_primary_10_1186_s41182_023_00552_6 crossref_primary_10_1016_j_freeradbiomed_2020_04_006 crossref_primary_10_1016_j_ijcard_2016_06_147 crossref_primary_10_1016_j_redox_2016_09_009 |
| Cites_doi | 10.1023/B:MCBI.0000009866.75225.e2 10.1016/j.cell.2007.01.047 10.1074/jbc.M112.374629 10.1042/BJ20101957 10.1016/S0735-1097(99)00630-0 10.1016/j.cardiores.2006.01.016 10.1113/jphysiol.2012.230185 10.1016/j.yjmcc.2006.07.008 10.1016/j.exger.2010.01.003 10.1152/ajpcell.00211.2007 10.4330/wjc.v3.i6.186 10.1515/bchm.1998.379.3.335 10.1152/ajpheart.00471.2001 10.1016/0009-8981(80)90192-8 10.1074/jbc.M510768200 10.1038/nprot.2008.61 10.1042/BJ20081386 10.1016/S0921-8777(99)00031-2 10.1152/ajpheart.1999.277.6.H2240 10.1152/physrev.00024.2007 10.1152/ajpheart.00992.2008 10.1056/NEJM200003023420904 10.1006/jmcc.1993.1144 10.1016/j.biocel.2009.03.013 10.1016/j.ejcts.2005.11.024 10.1016/j.freeradbiomed.2005.10.043 10.1016/j.mito.2011.02.001 10.1016/j.bbrc.2010.05.137 10.1093/eurjhf/hfs172 10.1007/978-1-61779-382-0_3 10.1016/j.jtcvs.2010.08.061 10.1016/j.bbabio.2005.10.003 |
| ContentType | Journal Article |
| Copyright | Copyright American Physiological Society Jun 1, 2013 |
| Copyright_xml | – notice: Copyright American Physiological Society Jun 1, 2013 |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 7QP 7QR 7TS 7U7 8FD C1K FR3 P64 7X8 |
| DOI | 10.1152/ajpheart.00991.2012 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed Calcium & Calcified Tissue Abstracts Chemoreception Abstracts Physical Education Index Toxicology Abstracts Technology Research Database Environmental Sciences and Pollution Management Engineering Research Database Biotechnology and BioEngineering Abstracts MEDLINE - Academic |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Technology Research Database Toxicology Abstracts Chemoreception Abstracts Engineering Research Database Calcium & Calcified Tissue Abstracts Physical Education Index Biotechnology and BioEngineering Abstracts Environmental Sciences and Pollution Management MEDLINE - Academic |
| DatabaseTitleList | MEDLINE - Academic Technology Research Database CrossRef MEDLINE |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine Anatomy & Physiology |
| EISSN | 1522-1539 |
| EndPage | H1414 |
| ExternalDocumentID | 2989462381 23542918 10_1152_ajpheart_00991_2012 |
| Genre | Research Support, Non-U.S. Gov't Journal Article Feature |
| GroupedDBID | --- 23M 2WC 39C 4.4 53G 5GY 5VS 6J9 AAFWJ AAYXX ABJNI ACBEA ACIWK ACPRK ADBBV AENEX AFRAH ALMA_UNASSIGNED_HOLDINGS BAWUL BKKCC BKOMP BTFSW CITATION E3Z EBS EJD EMOBN F5P GX1 H13 ITBOX KQ8 OK1 P2P PQQKQ RAP RHI RPL RPRKH TR2 UKR W8F WH7 WOQ XSW YSK ~02 CGR CUY CVF ECM EIF NPM 7QP 7QR 7TS 7U7 8FD C1K FR3 P64 7X8 |
| ID | FETCH-LOGICAL-c399t-ba169f18f091e46c85cd54f257a3b6dbc715e6de4f1862828f93c1bd73d1c2393 |
| ISSN | 0363-6135 1522-1539 |
| IngestDate | Thu Jul 10 19:04:04 EDT 2025 Mon Jun 30 17:13:24 EDT 2025 Thu Apr 03 06:57:24 EDT 2025 Thu Apr 24 23:02:29 EDT 2025 Tue Jul 01 01:16:17 EDT 2025 |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 11 |
| Keywords | left ventricle reactive oxygen species mitochondrial respiration |
| Language | English |
| LinkModel | OpenURL |
| MergedId | FETCHMERGED-LOGICAL-c399t-ba169f18f091e46c85cd54f257a3b6dbc715e6de4f1862828f93c1bd73d1c2393 |
| Notes | SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 |
| PMID | 23542918 |
| PQID | 1365275256 |
| PQPubID | 48261 |
| ParticipantIDs | proquest_miscellaneous_1365050569 proquest_journals_1365275256 pubmed_primary_23542918 crossref_primary_10_1152_ajpheart_00991_2012 crossref_citationtrail_10_1152_ajpheart_00991_2012 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2013-06-01 |
| PublicationDateYYYYMMDD | 2013-06-01 |
| PublicationDate_xml | – month: 06 year: 2013 text: 2013-06-01 day: 01 |
| PublicationDecade | 2010 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States – name: Bethesda |
| PublicationTitle | American journal of physiology. Heart and circulatory physiology |
| PublicationTitleAlternate | Am J Physiol Heart Circ Physiol |
| PublicationYear | 2013 |
| Publisher | American Physiological Society |
| Publisher_xml | – name: American Physiological Society |
| References | B20 B21 B22 Dos SP (B12) 2004; 256 B23 B24 B25 B27 B28 B29 Osterholt M (B26) 2012 B30 B31 B10 B32 B11 B33 B13 B14 B15 B16 B17 B18 B19 B1 B2 B3 B4 B5 B6 B7 B8 B9 |
| References_xml | – volume: 256 start-page: 157 year: 2004 ident: B12 publication-title: Mol Cell Biochem doi: 10.1023/B:MCBI.0000009866.75225.e2 – ident: B14 doi: 10.1016/j.cell.2007.01.047 – ident: B31 doi: 10.1074/jbc.M112.374629 – ident: B27 doi: 10.1042/BJ20101957 – ident: B10 doi: 10.1016/S0735-1097(99)00630-0 – ident: B11 doi: 10.1016/j.cardiores.2006.01.016 – ident: B19 doi: 10.1113/jphysiol.2012.230185 – ident: B21 doi: 10.1016/j.yjmcc.2006.07.008 – ident: B5 doi: 10.1016/j.exger.2010.01.003 – ident: B8 doi: 10.1152/ajpcell.00211.2007 – ident: B28 doi: 10.4330/wjc.v3.i6.186 – ident: B25 doi: 10.1515/bchm.1998.379.3.335 – ident: B4 doi: 10.1152/ajpheart.00471.2001 – ident: B13 doi: 10.1016/0009-8981(80)90192-8 – ident: B1 doi: 10.1074/jbc.M510768200 – ident: B18 doi: 10.1038/nprot.2008.61 – ident: B24 doi: 10.1042/BJ20081386 – ident: B22 doi: 10.1016/S0921-8777(99)00031-2 – ident: B2 doi: 10.1152/ajpheart.1999.277.6.H2240 – ident: B23 doi: 10.1152/physrev.00024.2007 – year: 2012 ident: B26 publication-title: Heart Fail Rev – ident: B16 doi: 10.1152/ajpheart.00992.2008 – ident: B20 doi: 10.1056/NEJM200003023420904 – ident: B33 doi: 10.1006/jmcc.1993.1144 – ident: B15 doi: 10.1016/j.biocel.2009.03.013 – ident: B3 doi: 10.1016/j.ejcts.2005.11.024 – ident: B7 doi: 10.1016/j.freeradbiomed.2005.10.043 – ident: B6 doi: 10.1016/j.mito.2011.02.001 – ident: B9 doi: 10.1016/j.bbrc.2010.05.137 – ident: B32 doi: 10.1093/eurjhf/hfs172 – ident: B29 doi: 10.1007/978-1-61779-382-0_3 – ident: B17 doi: 10.1016/j.jtcvs.2010.08.061 – ident: B30 doi: 10.1016/j.bbabio.2005.10.003 |
| SSID | ssj0005763 |
| Score | 2.1991205 |
| Snippet | Chronic ischemic heart disease is associated with myocardial hypoperfusion. The resulting hypoxia potentially inflicts damage upon the mitochondria, leading to... |
| SourceID | proquest pubmed crossref |
| SourceType | Aggregation Database Index Database Enrichment Source |
| StartPage | H1407 |
| SubjectTerms | 3-Hydroxyacyl CoA Dehydrogenases - metabolism Aged Blood Glucose - metabolism Blotting, Western Cardiomyocytes Cholesterol - blood Chronic Disease Coronary Artery Bypass Electron Transport - physiology Female Heart Human subjects Humans Hydrogen Peroxide - metabolism Hydroxyproline - metabolism Hypoxia Ischemia Ischemic Preconditioning, Myocardial Kinetics Lipids - blood Male Mitochondria Mitochondria, Heart - metabolism Myocardial Ischemia - metabolism Myocardial Ischemia - surgery Oxidative Phosphorylation Oxygen Consumption - physiology Phosphorylation Prostaglandin-Endoperoxide Synthases - metabolism Reactive Oxygen Species - metabolism Superoxide Dismutase - biosynthesis |
| Title | Impaired mitochondrial function in chronically ischemic human heart |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/23542918 https://www.proquest.com/docview/1365275256 https://www.proquest.com/docview/1365050569 |
| Volume | 304 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lb9NAEF6FIiEuCFqgoQUtEuICDvHbPlZVqwBpAJFIuVnel2SUOlVwpIZfz8w-7EQKqHCxkvU6dnZmPs_MzoOQNxnjosxTjMMZDr0I3jFeCWT2WBqKYSgzzEfHaItJMppFn-bxvNe73YpaWjdswH_tzSv5H6rCGNAVs2T_gbLtj8IAfAb6whEoDMc70fgjyHKFAeTXIJeAY7XQPTjwXeViGLkpflsuFpt3FViyOhbeNObDXtY7nvl292arnIT2fGjX-wBTllYmIJ1XK4xf1Rv03YzWW9OsKlPNd1K1KvsYLGgDcd8b2eWfjeTGu1rCP7QnTVmDDhfduCmCUNWl3TuyjgrdNMI5Kiy2gt0LAGsQUu4Zs4AcmobEjvP8LXwdgT2Y7kf-GCvJlj9u9OINUPNF89_GaO_U2Z58KS5n43ExvZhP75H7ARgYiJCfv3V15sEK06kZ7vFsvSr4_mHPLXZ1mj8YKlphmT4mj6ylQc8M2zwhPVkfkqOzGqh2vaFv6deWbofkwZUNsTgi546p6A5TUcdUtKrpFlNRx1RUMxXVD_2UzC4vpucjz3ba8DgoqI3HSj_JlZ8p0B5llHAU0ThSAOdlyBLBeOrHMhEygjkJGukqD7nPBAi0z7GI3jNyUC9reUzoMCv9kIW-UkJESS5ZpLjIZaZiJVUieJ8Ebq0KbsvQYzeURaHN0Tgo3AIXeoELXOA-ed9edGOqsPx9-qkjQmEl5meB8ZxBGoOK3yev29MAprhDVtZyuTZzsLVjkvfJc0O89n5BiK3d_OzFHa4-IQ87CTglB81qLV-C8tqwV5rPfgN8G57X |
| linkProvider | Colorado Alliance of Research Libraries |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Impaired+mitochondrial+function+in+chronically+ischemic+human+heart&rft.jtitle=American+journal+of+physiology.+Heart+and+circulatory+physiology&rft.au=Stride%2C+Nis&rft.au=Larsen%2C+Steen&rft.au=Hey-Mogensen%2C+Martin&rft.au=Hansen%2C+Christina+N&rft.date=2013-06-01&rft.issn=1522-1539&rft.eissn=1522-1539&rft.volume=304&rft.issue=11&rft.spage=H1407&rft_id=info:doi/10.1152%2Fajpheart.00991.2012&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0363-6135&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0363-6135&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0363-6135&client=summon |