The oxygen consumption paradox of “stunned myocardium” in dogs
dc.contributor.author | Shlafer, Marshal | en_US |
dc.contributor.author | Nicklas, John M. | en_US |
dc.contributor.author | Dean, Edward N. | en_US |
dc.date.accessioned | 2006-09-08T19:35:41Z | |
dc.date.available | 2006-09-08T19:35:41Z | |
dc.date.issued | 1990-03 | en_US |
dc.identifier.citation | Dean, E. N.; Shlafer, M.; Nicklas, J. M.; (1990). "The oxygen consumption paradox of “stunned myocardium” in dogs." Basic Research in Cardiology 85(2): 120-131. <http://hdl.handle.net/2027.42/41748> | en_US |
dc.identifier.issn | 1435-1803 | en_US |
dc.identifier.issn | 0300-8428 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/41748 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=2350326&dopt=citation | en_US |
dc.description.abstract | The contractile state of the heart is a major determinant of myocardial oxygen consumption. Since regional myocardial contractility can be severely impaired following a transient coronary occlusion, post-ischemic myocardium is frequently assumed to consume less oxygen. To test this assumption, regional myocardial function and oxygen consumption were studied in ancsthetized dogs during 2 h of myocardial reperfusion following either a 15-min (Group I) or 4-h (Group II) left anterior descending coronary artery occlusion. Both groups developed similar post-ischemic regional dysfunction characterized by paradoxical motion (negative shortening). Measured as a percent of baseline segment shortening, anterior wall function in Group I (n=8) and Group II (n=5) at 30 min of reperfusion was −33±11% and −34±16% (p=NS) and at 120 min was −23±9% and −40±16% (p=NS). However, the two groups showed a marked difference in regional myocardial oxygen consumption during reperfusion. Despite the abnormal wall motion, regional oxygen consumption in Group I at 30 and 120 min of reperfusion was unchanged from pre-ischemic levels as measured as a percent of bascline: 104±20% (p=NS) and 111±21% (p=NS). In contrast, regional oxygen consumption in Group II was markedly depressed from bascline at 30 and 120 min of reperfusion: 42±7% (p<.01) and 40±8% (p<.01). To determine whether the dissociation between regional myocardial oxygen consumption and function in Group I was related to mitochondrial uncoupling, six additional dogs were studied. Tissue samples were obtained from post-ischemic myocardium after 120 min of reperfusion following a 15-min coronary artery occlusion, and compared to non-ischemic myocardium. There were no differences in the in vitro mitochondrial respiratory rates or oxidative phosphorylation capacity between the post-ischemic and non-ischemic myocardium. Therefore, in the post-ischemic myocardium, significant depressions in regional contractility may not be associated with falls in oxygen consumption. Following a 15-min coronary artery occlusion, the injured myocardium maintains a paradoxically high oxygen consumption with normal mitochondrial function despite decreased contractility and abnormal wall motion. | en_US |
dc.format.extent | 864233 bytes | |
dc.format.extent | 3115 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Steinkopff-Verlag; Dr. Dietrich Steinkopff Verlag ; Springer Science+Business Media | en_US |
dc.subject.other | M Yocardial Ischemia | en_US |
dc.subject.other | Medicine & Public Health | en_US |
dc.subject.other | R Eperfusion | en_US |
dc.subject.other | O Xygen Consumption | en_US |
dc.subject.other | R Egional M Yocardial D Ysfunction | en_US |
dc.subject.other | M Itochondrial Oxidative P Hosphorylation | en_US |
dc.subject.other | Cardiology | en_US |
dc.title | The oxygen consumption paradox of “stunned myocardium” in dogs | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Oncology and Hematology | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Departments of Internal Medicine, Cardiology Division, Pharmacology, and Surgery, Thoracic Section, The University of Michigan, Ann Arbor, Michigan, USA | en_US |
dc.contributor.affiliationum | Departments of Internal Medicine, Cardiology Division, Pharmacology, and Surgery, Thoracic Section, The University of Michigan, Ann Arbor, Michigan, USA; 3910 Taubman Health Care Center, 1500 E. Medical Center Drive, 48109-0366, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationum | Departments of Internal Medicine, Cardiology Division, Pharmacology, and Surgery, Thoracic Section, The University of Michigan, Ann Arbor, Michigan, USA | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 2350326 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/41748/1/395_2005_Article_BF01906965.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1007/BF01906965 | en_US |
dc.identifier.source | Basic Research in Cardiology | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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