Figure 6
Figure 6. Influence of the A2BAR agonist (BAY 60-6583) on vascular permeability in bone marrow chimeric mice. A2BAR bone marrow chimeric mice (A: A2BAR−/−→A2BAR+/+; B: A2BAR+/+→A2BAR−/−) were treated with the selective A2BAR agonist (BAY 60-6583, 80 μg/kg intraperitoneally) or an equal volume of PBS 30 minutes before intravenous Evan blue dye (0.2 mL of 0.5% in PBS) and exposed to room air or normobaric hypoxia (8% O2, 92% N2) for 4 hours. Animals were killed and the heart (Ht), colon (Co), kidney (Kd), lung (Lg), spleen (Sp), brain (Br), muscle (Mu) and liver (Lv) were harvested. Organ Evan blue dye concentrations were quantified after formamide extraction (55°C for 2 hours) as described in “In vivo hypoxia model.” Data are expressed as means plus or minus SD of Evans blue OD/50 mg wet tissue (n = 6 animals/condition). (A: *P < .05, compared with normoxia; **P < .05, compared with −BAY 60-6583 control; and #P < .05, compared with −BAY 60-6583 control and normoxia; B: *P < .05, compared with normoxia).

Influence of the A2BAR agonist (BAY 60-6583) on vascular permeability in bone marrow chimeric mice.A2BAR bone marrow chimeric mice (A: A2BAR−/−A2BAR+/+; B: A2BAR+/+A2BAR−/−) were treated with the selective A2BAR agonist (BAY 60-6583, 80 μg/kg intraperitoneally) or an equal volume of PBS 30 minutes before intravenous Evan blue dye (0.2 mL of 0.5% in PBS) and exposed to room air or normobaric hypoxia (8% O2, 92% N2) for 4 hours. Animals were killed and the heart (Ht), colon (Co), kidney (Kd), lung (Lg), spleen (Sp), brain (Br), muscle (Mu) and liver (Lv) were harvested. Organ Evan blue dye concentrations were quantified after formamide extraction (55°C for 2 hours) as described in “In vivo hypoxia model.” Data are expressed as means plus or minus SD of Evans blue OD/50 mg wet tissue (n = 6 animals/condition). (A: *P < .05, compared with normoxia; **P < .05, compared with −BAY 60-6583 control; and #P < .05, compared with −BAY 60-6583 control and normoxia; B: *P < .05, compared with normoxia).

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