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Reduction of the edema of acute hyperoxic lung injury by granulocyte depletion
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1982
Year
Acute Lung InjuryAsthmaLung InflammationImmunologyGranulocyte DepletionEdematous Lung InjuryOxidative StressInflammationRespiratory ToxicologyIncreased NumbersHematologyPulmonary PharmacologyToxicologyNitrogen MustardTissue InjuryGranulocytePulmonary DiseaseInhalation ToxicologyMedicineEmergency Medicine
Increased numbers of granulocytes are found in lungs acutely injured by hyperoxia, but their contribution to lung injury remains unknown. We found that circulating granulocytes markedly increased (P less than 0.01) in rabbits exposed to hyperoxia for 72 h and that the numbers of granulocytes in lung lavages also increased and were correlated (r = 0.72, P less than 0.01) with the degree of edematous lung injury. Furthermore, when rabbits were treated with nitrogen mustard (1.75 mg/kg) and developed sustained granulocytopenia, exposure to hyperoxia for 72 h resulted in fewer granulocytes in lung lavages and less edematous lung injury. In contrast, when rabbits were similarly treated with nitrogen mustard but did not maintain sustained granulocytopenia throughout the exposure to hyperoxia, increased numbers of granulocytes were found in lung lavages and the degree of edematous lung injury increased to levels not different from those observed in oxygen-exposed rabbits that had not been treated with nitrogen mustard. These findings suggest that granulocytes may contribute to production of edema in acute oxygen toxicity.