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Acute hyperoxic lung edema is not reduced by granulocyte depletion in rats.

In order to study the role of neutrophils in hyperoxic lung edema, we induced a sustained granulocytopenia in rats by giving them a single intraperitoneal injection of 50 mg · kg”1 cyclophosphamide (CY) (CY-injected rats). Hyperoxic lung damage (FIO2 = 1.0, 60 h) was assessed by measuring pulmonary water (PW). Exposure to hyperoxia coincided with the granulocytopenic period. After exposure to hyperoxia, the difference in PW between CY- and 0.09% saline solution-injected (S-injected) rats was not significant (PW (g) (x ± 1 SD): CY-injected rats: 1.49 ± 0.09; S-injected rats: 1.68 ± 0.09, NS). If neutrophils have a pathogenic role in hyperoxic lung injury, the absence of edema reduction in neutropenic rats could be explained by pulmonary infection, insufficient neutrophil depletion or cumulative lung toxicity of CY and oxygen. No pulmonary infectious agents could be detected in lung and bronchoalveolar lavage cultures. Although already severe, the neutrophil depletion was intensified by a second injection of CY (50 mg · kg”1). After exposure to hyperoxia, the number of neutrophils in lung lavage was much lower in these neutropenic rats (156 · 103 ± 33 · 103) than in S-injected rats (571 103 ± 100–103) (p