Vascular permeability in A1, A2A, A2B and A3 adenosine receptor (AR)-deficient mice during hypoxia in vivo. (A) A1AR^−/−, (B) A2AAR^−/−, (C) A2BAR^−/−, or (D) A3AR^−/− mice and age-, weight-, and sex-matched littermate controls were exposed to room air (▭) or normobaric hypoxia (, 8% O₂, 92% N₂) for 4 hours and lung water content was measured. In additional studies, mice were administered intravenous Evan blue dye (0.2 mL of 0.5% in PBS) prior to hypoxia or normoxia exposure. Animals were killed and the heart (Ht), colon (Co), kidney (Kd), lung (Lg), spleen (Sp), brain (Br), muscle (Mu) and liver were harvested. Organ Evan blue dye concentrations were quantified as described in “In vivo hypoxia model.” Data are expressed as means plus or minus SD Evan blue OD/50 mg wet tissue; n = 6 animals/condition (*P < .05, compared with normoxia; **P < .05, compared with littermate controls; and #P < .05, compared with littermate controls and normoxia).