We have previously reported that administration of dexamethasone immediately prior to exposure to hyperoxia led to enhanced lung inflammation associated with earlier development of hyperoxic lung injury without increasing the lung expression of the proinflammatory adhesion molecules, E-Selectin and intercellular adhesion molecule-1. The purpose of this study was to determine whether administration of dexamethasone led to more rapid increases in lung P-Selectin expression in the course of hyperoxia-exposure. We administered 1 mg/kg of dexamethasone, or vehicle ip to adult rats immediately prior to hyperoxia-exposure. At 24, and 48 h of exposure, lungs were obtained and in-situ hybridizations carried out using an antisense probe to rat P-Selectin. Lung injury was also assessed by measuring extravascular lung water. In-situ hybridizations for P-Selectin were assessed for number of vessels positive for P-Selectin mRNA expression in 10 randomly selected high-powered fields. P-Selectin mRNA expression was higher as early as after 24 h of hyperoxia-exposure in animals given dexamethasone than in animals given vehicle alone, and was even higher after 48 of exposure to dexamethasone and hyperoxia. Extravascular lung water was higher in animals exposed to dexamethasone and hyperoxia than in vehicle and hyperoxia at 48 h of exposure. In conclusion, dexamethasone leads to earlier upregulation of P-Selectin mRNA in hyperoxic rat lungs and may contribute to the earlier lung inflammation and injury in hyperoxia-exposed rat lungs. *P<0.05, and **P<0.01 Table

Table 1 No caption available.
Full size table