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Am J Physiol Heart Circ Physiol (January 14, 2005). doi:10.1152/ajpheart.01081.2004
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Submitted on October 25, 2004
Accepted on January 12, 2005

Low Pressure Reperfusion Alters Mitochondrial Permeability Transition

Jean-Chrisostome Bopassa1, Pierre Michel1, Odile Gateau-Roesch2, Michel Ovize2*, and Rene Ferrera1

1 Inserm E0226, Lyon, France
2 Inserm E0226, Lyon, France; Hospices Civils de Lyon, Lyon, France

* To whom correspondence should be addressed. E-mail: ovize{at}sante.univ-lyon1.fr.

We hypothesized that low pressure reperfusion may limit myocardial necrosis and attenuate postischemic contractile dysfunction by inhibiting mitochondrial permeability transition pore (mPTP) opening. Male Wistar rats hearts (n=36) were perfused according to the Langendorff technique, exposed to 40 min of ischemia and assigned to one of the two following groups: (1) reperfusion with normal pressure (NP=100 cm H20) or (2) reperfusion with low pressure (LP=70 cm H2O). CK release and TTC staining evaluated infarct size. Modifications of cardiac function were assessed by changes in coronary flow (CF), heart rate (HR), left ventricular developed pressure (LVDP), the first derivate of the pressure curve (dP/dt) and rate-pressure product (RPP=LVDP.HR). Mitochondria were isolated from the reperfused myocardium and the Ca2+-induced mPTP opening was measured using a potentiometric approach. Lipid peroxidation was assessed by measuring malondialdehyde (MDA) production. Infarct size was significantly reduced in LP, averaging 17±3% versus 33±3% of the LV weight in NP hearts. At the end of reperfusion, functional recovery was significantly improved in LP hearts with RPP averaging 10392±876 mmHg/min versus 3969±534 mmHg/min in NP hearts (p<0.001). Ca2+ load required to induce mPTP opening averaged 232±10 µmoles in LP versus 128±16 µmoles in NP (p<0.001). Myocardial MDA was significantly lower in LP than in NP group (p<0.05). These results suggest that the protection afforded by low-pressure reperfusion involves an inhibition of the opening of the mitochondrial permeability transition pore, possibly via reduction of reactive oxygen species production.




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