Hyperoxia and Lung ~etabol ism*

N umerous studies have been conducted on the pathologic changes that occur in the lung due to exposure to hyperbaric oxygen. These studies indicate that the entire lung, from the epithelium of the upper respiratory tract down to the pulmonary capillary endothelium, can be damaged by prolonged exposure to elevated partial pressures of oxygen.' Reports of 2-4 lung tissue changes due to oxygen toxicity include interstitial and intracellular edema, thickening of the oxygen blood barrier, and swelling of mitochondria in the alveolar epithelium. Indirect mechanisms as well as the direct effects of oxygen can be responsible for the damage observed in lung tissue. In vitro studies have shown that many enzymes are inhibited by exposure to hyperbaric oxygen in the absence of hormonal and neurogenic factor^.^ Penrode reported in studies in which only one lung was exposed to the effects of elevated oxygen tensions that damage occurred in the absence of extrapulmonary factors. Studies on biochemical damage that occurs in the lung due to pulmonary oxygen toxicity are not numerous and little is known about biochemical changes that occur in the lungs of intact animals during exposure to subconvulsive levels of hyperbaric oxygen. After 15 to 30 minutes of breathing oxygen at 5.0 atmospheres absolute pressure ( ATA) , dehydrogenase activity and sulfhydryl content of lung tissue are significantly decreased.7 Other investigatorsR have reported that cats exposed to 100 percent oxygen showed a marked impairment of tracheal mucus flow, which could be reversed by administering epinephrine and adenosine tiphosphate ( ATP) . The authors0 interpreted the effect of oxygen on mucus flow as an interference by oxygen on carbohydrate metabolism. Proposals as to the mechanism of pulmonary oxygen toxicity include enzyme inhibition, free radical formation, and peroxidation. Previous pa;hologic and biochemical studies have shown that significant damage occurs in the lung due to oxygen toxicity. We found biochemical changes occurring in the lung of rats exposed to 1.0 ATA 160 percent 0, from zero to seven days. Pathologic changes in the lung were monitored, simultaneously. Succinic dehydrogenase activity, basal and ADP-stimulated respiration rates, and ATP concentrations were measured.