PULMONARY INFLAMMATION DUE TO OXYGEN-TOXICITY - INVOLVEMENT OF CHEMOTACTIC FACTORS AND POLYMORPHONUCLEAR LEUKOCYTES

Abstract

Although the pathogenesis of pulmonary O2 toxicity is not fully understood, the fact that increased numbers of polymorphonuclear leukocytes (PMN) are found in the lung coinciding with the massive endothelial damage suggests that PMN may contribute to lung injury caused by hyperoxia. To elucidate a mechanism for this influx of PMN chemoattractant activity for PMN was measured in lung lavages of rats exposed to > 95% O2 for various durations. Chemoattractant activity of the lung lavages of rats exposed to hyperoxia for 66 h was markedly increased (9.66 .+-. 1.0 times) compared to activities in lavages of normoxic control rats. These increases in chemoattractant activity in lung lavages correlated well with increases in the number of PMN (7 times that in normoxic control animals) in the alveolar lavages that occurred after the rats were exposed to hyperoxia for 66 h. These increases were followed in a few hours by the death of most of the rats (71%). Apparently, a close temporal relationship exists between the generation of high concentrations of chemoattractants in lung lavages, PMN influx into lung lavages and death of rats exposed to hyperoxia. PMN may be involved in the pathogenesis of pulmonary O2 toxicity.