Influence of dCF on pulmonary edema, vascular permeability, and PMN accumulation in vivo. BL/6/129 mice were given injections of dCF (1 mg/kg intraperitoneally and 1 mg/kg subcutaneously) or PBS, and exposed to normoxia (room air) or normobaric hypoxia (8% O₂ and 92% N₂) for 4 hours. (A) Assessment of lung water content in normoxia (▪) and hypoxia () after dCF or PBS treatment. Data are expressed as mean ± SD mg H₂O/mg dry tissue, and are pooled from 6 animals per condition. ^*Significantly different between hypoxia and normoxia (P < .025). #Significantly different between dCF treatment and vehicle control (P < .025). (B) To assess vascular barrier function, animals were administered intravenous Evan blue dye solution (0.2 mL of 0.5% in PBS) prior to normoxia/hypoxia exposure. Animals were killed, and the lung, colon, and liver were harvested. Organ Evan blue concentrations were quantified following formamide extraction (55°C for 2 hours) by measuring absorbances at 610 nm with subtraction of reference absorbance at 450 nm. Data are expressed as mean ± SD Evan blue optical density (OD)/50mg wet tissue, and are pooled from 6 animals per condition. Note that Evan blue retention increases with hypoxia and decreases with dCF treatment. ^*Significant differences between normoxia/hypoxia exposure (P < .01). #Significant differences between dCF/PBS treatment groups (P < .025). (C) Organ assessment of PMN accumulation by myeloperoxidase (MPO) measurements in the indicated organs after 4 hours of normoxia/hypoxia exposure (^*P < .01 compared with hypoxia; #P < .025 compared with vehicle control). Error bars indicate SD.