AJP - Heart Calcium Transients and Cell-Sarcomere
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 287: H258-H267, 2004. First published February 26, 2004; doi:10.1152/ajpheart.00348.2003
0363-6135/04 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
287/1/H258    most recent
00348.2003v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (14)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lesnefsky, E. J.
Right arrow Articles by Hoppel, C. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lesnefsky, E. J.
Right arrow Articles by Hoppel, C. L.

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

Edward J. Lesnefsky,1,5 Qun Chen,1 Thomas J. Slabe,5 Maria S. K. Stoll,5 Paul E. Minkler,5 Medhat O. Hassan,6 Bernard Tandler,4 and Charles L. Hoppel2,3,5

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


Address for reprint requests and other correspondence: E. J. Lesnefsky, Cardiology Section, Medical Service 111(W), Louis Stokes VA Medical Center, 10701 East Blvd., Cleveland, OH 44106 (E-mail: EXL9{at}cwru.edu).




This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
J. D. McCully, D. B. Cowan, C. A. Pacak, I. K. Toumpoulis, H. Dayalan, and S. Levitsky
Injection of isolated mitochondria during early reperfusion for cardioprotection
Am J Physiol Heart Circ Physiol, January 1, 2009; 296(1): H94 - H105.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
T. Nguyen, M. Ogbi, and J. A. Johnson
Delta Protein Kinase C Interacts with the d Subunit of the F1F0 ATPase in Neonatal Cardiac Myocytes Exposed to Hypoxia or Phorbol Ester: IMPLICATIONS FOR F1F0 ATPase REGULATION
J. Biol. Chem., October 31, 2008; 283(44): 29831 - 29840.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
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]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
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]

Home page
 Am. J. Physiol. Cell Physiol.Home page
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]

Home page
 Am. J. Physiol. Cell Physiol.Home page
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]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2004 by the American Physiological Society.