Abstract
It has been proposed that activation of the mitochondrial ATP-sensitive potassium channel (mitoKATP) is part of signaling pathways triggering the cardioprotection afforded by ischemic preconditioning of the heart. This work was to analyze the mitochondrial function profile of Langendorff-perfused rat hearts during the different phases of various ischemia-reperfusion protocols. Specifically, skinned fibers of ischemic preconditioned hearts exhibit a decline in the succinate-supported respiration and complex II activity during ischemia, followed by a recovery during reperfusion. Meanwhile, the apparent affinity of respiration for ADP (which reflects the matrix volume expansion) is increased during preconditioning stimulus and, to a larger extent, during prolonged ischemia. This evolution pattern is mimicked by diazoxide and abolished by 5-hydroxydecanoate. It is concluded that opening the mitoKATP channel mediates the preservation of mitochondrial structure-function via a mitochondrial matrix shrinkage and a reversible inactivation of complex II during prolonged ischemic insult.
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Pasdois, P., Beauvoit, B., Tariosse, L. et al. MitoK ATP -dependent changes in mitochondrial volume and in complex II activity during ischemic and pharmacological preconditioning of langendorff-perfused rat heart. J Bioenerg Biomembr 38, 101–112 (2006). https://doi.org/10.1007/s10863-006-9016-3
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DOI: https://doi.org/10.1007/s10863-006-9016-3