Abstract

Opening of a large conductance channel in the inner mitochondrial membrane, known as the mitochondrial permeability transition (MPT) pore, has been shown to be a primary mediator of cell death in the heart subjected to ischemia-reperfusion injury. Inhibitors of the MPT have been shown to reduce cardiac ischemia-reperfusion injury. Furthermore, most cardioprotective strategies appear to reduce ischemic cell death either by reducing the triggers for the opening of the MPT, such as reducing calcium overload or reactive oxygen species, or by more direct inhibition of the MPT. This chapter focuses on key issues in the study of the MPT and provides some methods for measuring MPT opening in isolated mitochondria.

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