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Depolarized Mitochondrial Membrane Potential and Protection with Duroquinone in Isolated Perfused Lungs from Rats Exposed to Hyperoxia

Dissipation of mitochondrial membrane potential (Δψm) is a hallmark of mitochondrial dysfunction, which plays a key in the pathogenesis of Acute Respiratory Distress Syndrome (ARDS). Our objective was to use a previously developed experimental‐computational approach to estimate tissue Δψm in isolated perfused lungs of rats exposed to hyperoxia as a rat model of human ARDS, and to evaluate the ability of the ubiquinone analog duroquinone (DQ) to reverse any hyperoxia‐induced depolarization of lung Δψm.