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1 EMI-U 226, INSERM, LYON, France
2 EMI-U 226, INSERM, LYON, France; IRCV, Bourgogne University, DIJON, France
* To whom correspondence should be addressed. E-mail: ferrera{at}lyon.inserm.fr.
Objective. We investigated whether low-pressure reperfusion may attenuate postischemic contractile dysfunction, limits necrosis and apoptosis after a prolonged hypothermic ischemia and inhibits mitochondrial permeability transition pore (MPTP) opening. Method. Isolated rats hearts (n=72) were exposed to 8 hours of cold ischemia and assigned to the following groups: (1) reperfusion with low pressure (LP=70 cm H2O); (2) reperfusion with normal pressure (NP=100 cm H20). Cardiac function was assessed during reperfusion using Langendorff model. Mitochondria were isolated and the Ca2+ resistance capacity (CRC) of the MPTP was determined. Malondialdehyde (MDA) production, caspase-3 activity and cytochrome C were also assessed. Result. Functional recovery was significantly improved in LP hearts with rate-pressure product averaging 30380±1757 mmHg/min versus 18000±1599 mmHg/min in NP hearts (p<0.01). Necrosis, measured by TTC staining and CK leakage, was significantly reduced in LP hearts (p<0.01). The CRC was increased in LP heart mitochondria (p<0.01). Caspase-3 activity, cytochrome C release and MDA production were reduced in LP hearts (respectively, p<0.001 and p<0.01). Conclusion. This study demonstrated that low-pressure reperfusion following hypothermic heart ischemia improves postischemic contractile dysfunction and attenuates necrosis and apoptosis. This protection could be related to an inhibition of mitochondrial permeability transition.
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