Pasdois 2006 J Bioenerg Biomembr
|Pasdois P, Beauvoit B, Tariosse L, Vinassa B, Bonoron-Adèle S, Santos PD (2006) 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 38:101-12.
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. • Keywords: MitokATP, Diazoxide, Ischemic preconditioning, Succinate dehydrogenase, Complex II
• O2k-Network Lab: FR Pessac Diolez P
Stress:Ischemia-reperfusion Organism: Rat Tissue;cell: Heart Preparation: Permeabilized tissue
Coupling state: OXPHOS