Lung Energy Metabolism Following Twenty-Four Hours Exposure to One Hundred Percent Oxygen

The interstitial edema and endothelial cell damage observed in rat lungs following 48 hours of exposure to 100% oxygen is believed to result from oxygen-derived free-radical damage of cellular membranes, enzyme proteins, and possibly components of the extracellular matrix. Earlier physiological alterations of endothelial function have been demonstrated by depressed serotonin uptake in isolated perfused rat lungs following 18 to 24 hours of oxygen exposure,1 at a time when tissue adenine nucleotide levels have been found not to be affected.2 In vitro experiments using homogenates and isolated subcellular tissue fractions have demonstrated that key enzyme systems involved in energy generation are susceptible to oxygen inactivation. These include the dehydrogenases of glyceraldehyde-3-phosphate, pyruvate, succinate, and oxoglutarate.3–5 The purpose of the present investigation was to use an intact organ preparation to determine whether lung glycolytic and mitochondrial enzyme systems are impaired during the first 24 hours of oxygen exposure when pathological alterations are not observed.