Abstract

In vivo hyperoxic preconditioning (PC) has been shown to protect against ischemia/reperfusion (I/R)myocardial damage. Mitochondrial permeability transition pore (MPTP) opening is an important event incardiomyocyte cell death occurring during I/R and therefore a possible target for cardioprotection. We testedthe hypothesis that in vivo hyperoxic PC, obtained by mechanical ventilation of animals, could protect heartagainst I/R injury by inhibiting MPTP opening and cytochrome c release from mitochondria. Mechanicallyventilated rats were first exposed to a short period of hyperoxia and isolated hearts were subsequentlysubjected to I/R in a Langendorff apparatus. Hyperoxic PC significantly improved the functional recovery ofhearts on reperfusion, reduced the infarct size, and decreased necrotic damage as shown by the reducedrelease of lactate dehydrogenase. Mitochondria from hyperoxic PC hearts were less sensitive thanmitochondria from reperfused heart to MPTP opening. In addition, hyperoxic PC prevented mitochondrialNAD+ depletion, an indicator of MPTP opening, and cytochrome c release as well as cardiolipin oxidation/depletion associated with I/R. Together, these results demonstrate that hyperoxic PC protects against heart I/Rinjury by inhibiting MPTP opening and cytochrome c release. Thus, in vivo hyperoxic PC may represent auseful strategy for the treatment of cardiac I/R injury and could have potential applications in clinical practice.

Autore Pugliese

• Petrosillo Giuseppe

Tutti gli autori

• Petrosillo G.; Di Venosa N.; Moro N.; Colantuono G.; Paradies V.; Tiravanti E.A.; Federici A.; Ruggiero F.M.; Paradies G.

Titolo volume/Rivista

Free radical biology & medicine

Anno di pubblicazione

2011

ISSN

0891-5849

ISBN

Non Disponibile

Numero di citazioni Wos

Nessuna citazione

Ultimo Aggiornamento Citazioni

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Numero di citazioni Scopus

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Ultimo Aggiornamento Citazioni

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Settori ERC

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Codici ASJC

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