Document Detail

Remote ischemic preconditioning elaborates a transferable blood-borne effector that protects mitochondrial structure and function and preserves myocardial performance after neonatal cardioplegic arrest.
MedLine Citation:
PMID:  18692639     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: Remote ischemic preconditioning is known to elicit production of a blood-borne cardioprotective factor that is infarct sparing in models of ischemia-reperfusion injury and myocardial damage reducing after cardiopulmonary bypass in human subjects. The mechanism of protection remains incompletely understood. In this study, we examined effects on mitochondrial structure and function in a noninfarct model of cardioplegic arrest. METHODS: Explanted neonatal rabbit hearts were mounted in a Langendorff preparation and perfused with dialysate of blood taken from sham-treated or remotely preconditioned rabbits. Each heart was subsequently subjected to 1-hour cardioplegic arrest and 30-minute reperfusion periods, during which hemodynamic responses were measured. Mitochondria were isolated for structural and functional measurements. RESULTS: Relative to hearts with sham-treated dialysate, myocardial performance (systolic pressure, maximum positive and negative first derivatives of left ventricular pressure, and left ventricular end-diastolic pressure) was better preserved with dialysate from preconditioned rabbits. Similarly, mitochondria isolated from hearts with dialysate from preconditioned rabbits showed preserved respiration at complex I and IV in the electron transport chain (P < .01 and P < .05, respectively). Mitochondrial outer membrane integrity was also preserved, with diminished sensitivity of mitochondrial respiration to exogenous cytochrome c (P < .01) and less cytosolic diffusion of cytochrome c (P < .01). Mitochondrial resistance to calcium-mediated mitochondrial permeability transition pore opening was not affected. CONCLUSION: The cardioprotective factor in plasma dialysate after remote preconditioning preserves mitochondrial structure and function in a noninfarct cardioplegic arrest model. This protection is associated with preservation of global myocardial performance.
Lixing Wang; Norihiko Oka; Michael Tropak; John Callahan; John Lee; Greg Wilson; Andrew Redington; Christopher A Caldarone
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-06-02
Journal Detail:
Title:  The Journal of thoracic and cardiovascular surgery     Volume:  136     ISSN:  1097-685X     ISO Abbreviation:  J. Thorac. Cardiovasc. Surg.     Publication Date:  2008 Aug 
Date Detail:
Created Date:  2008-08-11     Completed Date:  2008-08-29     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0376343     Medline TA:  J Thorac Cardiovasc Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  335-42     Citation Subset:  AIM; IM    
Division of Cardiovascular Research, Hospital for Sick Children, Toronto, Ontario, Canada.
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MeSH Terms
Animals, Newborn
Calcium / metabolism
Cardiotonic Agents / metabolism*
Cytochromes c / metabolism,  pharmacology
Heart Arrest, Induced*
Ischemic Preconditioning, Myocardial*
Mitochondria, Heart / metabolism*
Mitochondrial Membrane Transport Proteins / metabolism
Mitochondrial Membranes / metabolism
Myocardial Reperfusion
Oxygen Consumption
Ventricular Function, Left*
Reg. No./Substance:
0/Cardiotonic Agents; 0/Mitochondrial Membrane Transport Proteins; 0/mitochondrial permeability transition pore; 7440-70-2/Calcium; 9007-43-6/Cytochromes c

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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