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International Journal of Physiology and Pathophysiology

Publicado 4 números por año

ISSN Imprimir: 2155-014X

ISSN En Línea: 2155-0158

SJR: 0.116

Mitochondrial Permeability Transition as a Target for Ischemic Preconditioning

Volumen 3, Edición 2, 2012, pp. 111-124
DOI: 10.1615/IntJPhysPathophys.v3.i2.20
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SINOPSIS

Ischemic preconditioning (IPC) has the ability to increase myocardial resistance to reperfusion injury. The mechanisms underlying myocardial adaptation to ischemia have being actively studied, while it is known with certainty that IPC stimulates effective restoration of mitochondrial energy producing function. The purpose of the present study was to clear up the ways of cardioprotective effect of IPC that is engaged in the regulation of mitochondrial membrane permeability and which mediates adaptation of the heart to ischemia. In experiments on Langendorf isolated rat hearts and cardiac mitochondria, it has been shown that three 5-minute episodes of IPC prevented an excessive production of reactive oxygen species during prolonged myocardial ischemia-reperfusion and provided an effective restoration of heart function. At that, we observed an inhibition of mitochondrial permeability transition pore opening due to increased NO synthesis. This was confirmed by decreasing the release of mitochondrial factors in the coronary flow and reducing susceptibility of isolated mitochondria to calcium ions after IPC. It has been concluded that among the processes involved in the cardioprotective effect of IPC, reduced mitochondrial membrane permeability due to blockade of mitochondrial permeability transition pore opening plays a crucial role.

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