Dexamethasone (DEX) is utilized as an antiinflammatory agent in the treatment of bronchopulmonary dysplasia (BPD). DEX has been shown, however, to accelerate lung injury in hyperoxia-exposed animals. We, therefore, studied the effects of DEX on the lung inflammatory responses of hyperoxia-exposed rats. We administered 1 mg/kg DEX or vehicle ip and placed rats in >95% O2. At 0, 24, and 48 h of hyperoxia-exposure, we collected whole blood for circulating neutrophil (PMN) counts and assessed myeloperoxidase (MPO) activity per PMN. At the same times lung samples for Western blot analysis of E-Selectin and ICAM-1 expression and for lung PMN counts were obtained. DEX treatment increased lung PMN counts independent of hyperoxia-exposure without a change in the expression of E-Selectin or ICAM-1. In addition, DEX-treatment decreased the MPO activity per PMN independent of hyperoxia-exposure. In conclusion, our findings suggest that dexamethasone augments the lung inflammatory response to hyperoxia-exposure by its effects on neutrophils rather than the vascular endothelium. Table

Table 1
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