HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 287/1/H258    most recent 00348.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (14) Citing Articles via Google Scholar Google Scholar Articles by Lesnefsky, E. J. Articles by Hoppel, C. L. Search for Related Content PubMed PubMed Citation Articles by Lesnefsky, E. J. Articles by Hoppel, C. L.

Ischemia, rather than reperfusion, inhibits respiration through cytochrome oxidase in the isolated, perfused rabbit heart: role of cardiolipin

Divisions of ¹Cardiology and ²Clinical Pharmacology, Department of Medicine, ³Department of Pharmacology, and ⁴Department of Oral Diagnosis, School of Dental Medicine, Case Western Reserve University, and ⁵Medical and ⁶Pathology and Laboratory Medicine Services, Louis Stokes Veterans Affairs Medical Center, Cleveland, Ohio 44106

Submitted 11 April 2003 ; accepted in final form 18 February 2004

Ischemia and reperfusion result in mitochondrial dysfunction, with decreases in oxidative capacity, loss of cytochrome c, and generation of reactive oxygen species. During ischemia of the isolated perfused rabbit heart, subsarcolemmal mitochondria, located beneath the plasma membrane, sustain a loss of the phospholipid cardiolipin, with decreases in oxidative metabolism through cytochrome oxidase and the loss of cytochrome c. We asked whether additional injury to the distal electron chain involving cardiolipin with loss of cytochrome c and cytochrome oxidase occurs during reperfusion. Reperfusion did not lead to additional damage in the distal electron transport chain. Oxidation through cytochrome oxidase and the content of cytochrome c did not further decrease during reperfusion. Thus injury to cardiolipin, cytochrome c, and cytochrome oxidase occurs during ischemia rather than during reperfusion. The ischemic injury leads to persistent defects in oxidative function during the early reperfusion period. The decrease in cardiolipin content accompanied by persistent decrements in the content of cytochrome c and oxidation through cytochrome oxidase is a potential mechanism of additional myocyte injury during reperfusion.

cytochrome c; oxygen radicals; phospholipids

This article has been cited by other articles:

				Q. Chen, S. Moghaddas, C. L. Hoppel, and E. J. Lesnefsky Ischemic defects in the electron transport chain increase the production of reactive oxygen species from isolated rat heart mitochondria Am J Physiol Cell Physiol, February 1, 2008; 294(2): C460 - C466. [Abstract] [Full Text] [PDF]

				D. H. Korzick, J. C. Kostyak, J. C. Hunter, and K. W. Saupe Local delivery of PKC{varepsilon}-activating peptide mimics ischemic preconditioning in aged hearts through GSK-3beta but not F1-ATPase inactivation Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2056 - H2063. [Abstract] [Full Text] [PDF]

				A. J. Chicco and G. C. Sparagna Role of cardiolipin alterations in mitochondrial dysfunction and disease Am J Physiol Cell Physiol, January 1, 2007; 292(1): C33 - C44. [Abstract] [Full Text] [PDF]

				Q. Chen, A. K. S. Camara, D. F. Stowe, C. L. Hoppel, and E. J. Lesnefsky Modulation of electron transport protects cardiac mitochondria and decreases myocardial injury during ischemia and reperfusion Am J Physiol Cell Physiol, January 1, 2007; 292(1): C137 - C147. [Abstract] [Full Text] [PDF]