Skip Navigation

Cardiovascular Research 2004 61(3):365-371; doi:10.1016/j.cardiores.2003.12.012
© 2004 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Piper, H.M
Right arrow Articles by Schäfer, C
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Piper, H.M
Right arrow Articles by Schäfer, C
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2003, European Society of Cardiology

The first minutes of reperfusion: a window of opportunity for cardioprotection

H.M Piper*, Y Abdallah and C Schäfer

Physiologisches Institut, Justus-Liebig-Universität, Aulweg 129, D-35392 Giessen, Germany

* Corresponding author. Tel.: +49-641-9947241; fax: +49-641-9947239. michael.piper{at}physiologie.med.uni-giessen.de

During the past decade, the understanding has grown that control of the conditions of reperfusion is critical for salvaging ischemic–reperfused myocardium. The first few minutes of reperfusion constitute a critical phase, as here lethal tissue injury in addition to that already developed during ischemia may be initiated. The identification of the mechanisms of reperfusion-induced cell death opens a new window of opportunity for cardioprotection in the clinic. Development of cardiomyocyte hypercontracture is a predominant feature of reperfusion injury. We and others have shown that control of hypercontracture in reperfusion reduces the extent of tissue injury. On the cellular level, it was shown that reperfusion-induced hypercontracture might either originate from a rigor-type mechanism, when energy recovery proceeds very slowly, or from Ca2+ overload, when energy recovery is rapid but cytosolic Ca2+ load is high. These two mechanisms can be influenced by various interventions that either connect with cytosolic Ca2+ control or myofibrillar Ca2+ sensitivity or with mitochondrial energy production. These experimental approaches will hopefully lead to novel strategies for clinical cardioprotection during the early phase of reperfusion.

KEYWORDS Calcium; Cardioprotection; Hypercontracture; Ischemia; Reperfusion


Time for primary review 15 days


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Cardiovasc ResHome page
L. Gomez, B. Li, N. Mewton, I. Sanchez, C. Piot, M. Elbaz, and M. Ovize
Inhibition of mitochondrial permeability transition pore opening: translation to patients
Cardiovasc Res, July 15, 2009; 83(2): 226 - 233.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
J. Inserte, J. A. Barrabes, V. Hernando, and D. Garcia-Dorado
Orphan targets for reperfusion injury
Cardiovasc Res, July 15, 2009; 83(2): 169 - 178.
[Abstract] [Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
J. D. O'Brien, S. E. Howlett, H. J. Burton, S. B. O'Blenes, D. S. Litz, and C. L. H. Friesen
Pediatric cardioplegia strategy results in enhanced calcium metabolism and lower serum troponin T.
Ann. Thorac. Surg., May 1, 2009; 87(5): 1517 - 1523.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
R. Whittaker, M. S. Glassy, N. Gude, M. A. Sussman, R. A. Gottlieb, and C. C. Glembotski
Kinetics of the translocation and phosphorylation of {alpha}B-crystallin in mouse heart mitochondria during ex vivo ischemia
Am J Physiol Heart Circ Physiol, May 1, 2009; 296(5): H1633 - H1642.
[Abstract] [Full Text] [PDF]


Home page
J. Thorac. Cardiovasc. Surg.Home page
U. Abdel-Rahman, P. Risteski, K. Tizi, S. Kerscher, S. Bejati, K. Zwicker, M. Scholz, U. Brandt, and A. Moritz
Hypoxic reoxygenation during initial reperfusion attenuates cardiac dysfunction and limits ischemia-reperfusion injury after cardioplegic arrest in a porcine model
J. Thorac. Cardiovasc. Surg., April 1, 2009; 137(4): 978 - 982.
[Abstract] [Full Text] [PDF]


Home page
J. Physiol.Home page
R. J. Solaro
Maintaining cooperation among cardiac myofilament proteins through thick and thin
J. Physiol., January 1, 2009; 587(1): 3 - 3.
[Full Text] [PDF]


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
Am. J. Physiol. Heart Circ. Physiol.Home page
E. Takahashi
Anoxic cell core can promote necrotic cell death in cardiomyocytes at physiological extracellular PO2
Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2507 - H2515.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
L. H. Opie
Metabolic Management of Acute Myocardial Infarction Comes to the Fore and Extends Beyond Control of Hyperglycemia
Circulation, April 29, 2008; 117(17): 2172 - 2177.
[Full Text] [PDF]


Home page
Physiol. Rev.Home page
E. Murphy and C. Steenbergen
Mechanisms Underlying Acute Protection From Cardiac Ischemia-Reperfusion Injury
Physiol Rev, April 1, 2008; 88(2): 581 - 609.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.