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| Remote ischemic preconditioning elaborates a transferable blood borne factor which protects mitochondrial structure and function and preserves myocardial performance after neonatal cardioplegic arrest |
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Norihiko Oka, Lixing Wang, Michael Tropek, John Callahan, Gregory Wilson, Andrew Redington, Christopher A. Caldarone; Hospital for Sick Children, Toronto, ON, Canada Objective: Remote ischemic preconditioning is known to elicit production of a blood borne cardioprotective factor with infarct-sparing effects in models of ischemia-reperfusion injury. The mechanism of protection remains incompletely understood. In this study we examine the effects of the cardioprotective factor on mitochondrial structure and function in a non-infarct model of cardioplegic arrest. Methods: Explanted neonatal rabbit hearts were mounted in a Langendorf preparation. The hearts were perfused with a dialysate of blood taken from another group of rabbits which were sham-treated or remotely preconditioned. Each heart was subsequently subjected to 1 hour of cardioplegic arrest and 30 minutes of reperfusion during which hemodynamic responses were measured. Mitochondria were then isolated for structural and functional measurements. Results: Compared to hearts treated with the sham-treated dialysate, myocardial performance (systolic pressure, maximum positive dP/dT, negative dP/dT, and LVEDP) was better preserved after treatment with dialysate from preconditioned rabbits. Similarly, mitochondria isolated from hearts treated with the dialysate from preconditioned rabbits showed preserved respiration at complex I and IV in the electron transport chain (P<0.01 and P<0.05 respectively). Mitochondrial outer membrane integrity was also preserved with diminished sensitivity of mitochondrial respiration to exogenous cytochrome c (P<0.01) and less diffusion of cytochrome c into the cytosol (P<0.01). Mitochondrial resistance to calcium-mediated mPTP opening was not affected. Conclusion: The cardioprotective factor present in plasma dialysate following remote preconditioning preserves mitochondrial structure and function in a non-infarct cardioplegic arrest model. This protection is associated with preservation of global myocardial performance. Back to 88th Annual Meeting Back to Program Outline |
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