Document Detail

Ischemic preconditioning preserves proton leakage from mitochondrial membranes but not oxidative phosphorylation during heart reperfusion.
MedLine Citation:
PMID:  16245370     Owner:  NLM     Status:  MEDLINE    
The aim of this study was to evaluate the role of mitochondria in the recovery of cardiac energetics induced by ischaemic preconditioning at reperfusion. Isolated rat hearts were aerobically perfused (control), subjected to global ischaemia and reperfusion (reperfusion), or subjected to 3 brief cycles of ischaemia/reperfusion and then to the protocol of reperfusion (preconditioning). At the end of the perfusion, antimycin A was delivered to the heart for 25 min, to inhibit mitochondrial respiration and stimulate glycolysis. The increased amount of lactate released in the coronary effluent was correlated with the number of viable cells producing this end-product of glycolysis. Preconditioned hearts released 18% more lactate than reperfused hearts (p < 0.05). This result indicates that preconditioning partially preserved cell viability, as was also evidenced by the MTT assay performed on cardiac biopsies. The difference between antimycin A-stimulated and basal lactate concentration, representing the contribution of mitochondria to the overall energetics of cardiac tissue, was also 18% more elevated in the preconditioned hearts than in the reperfused hearts (p < 0.01). The study of the respiratory function of mitochondria isolated at the end of perfusion, showed that preconditioning did not improve the oxygen-dependent production of ATP (state 3 respiration, ADP/O). On the contrary, state 4 respiration, which is related to proton leakage, was 35.0% lower in the preconditioned group than reperfusion group (p < 0.05). Thus, preconditioning ameliorates cardiac energetics by preserving cell death, but without affecting mitochondrial oxidative phosphorylation. Mitochondria can contribute to cell survival by the attenuation of proton leak from inner membrane.
Claudio Muscari; Francesca Bonafè; Chiara Gamberini; Emanuele Giordano; Giorgio Lenaz; Claudio Marcello Caldarera
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cell biochemistry and function     Volume:  24     ISSN:  0263-6484     ISO Abbreviation:  Cell Biochem. Funct.     Publication Date:    2006 Nov-Dec
Date Detail:
Created Date:  2006-10-25     Completed Date:  2007-02-08     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8305874     Medline TA:  Cell Biochem Funct     Country:  England    
Other Details:
Languages:  eng     Pagination:  511-8     Citation Subset:  IM    
Copyright Information:
Copyright (c) 2005 John Wiley & Sons, Ltd.
Department of Biochemistry G. Moruzzi, University of Bologna, Via Irnerio 48, 40126 Bologna, Italy.
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MeSH Terms
Biological Transport, Active
Cell Respiration
Cell Survival
Intracellular Membranes / metabolism*
Ischemic Preconditioning*
Lactic Acid / biosynthesis
Mitochondria / metabolism*
Myocardial Reperfusion Injury / metabolism*,  prevention & control*
Oxidative Phosphorylation*
Rats, Wistar
Reg. No./Substance:
0/Protons; 50-21-5/Lactic Acid

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