Figure 4
Figure 4. ATL146e treatment decreases pulmonary dysfunction in NY1DD mice by activation of the A2AR. C57BL/6, NY1DD, or NY1DD x A2AR−/− mice were treated with ATL146e (10 ng/kg/minute, 3 days) or vehicle (saline, 0.2% DMSO). (A-F) Lung sections from NY1DD mice, but not NY1DD x A2AR−/− mice have reduced alveolar thickening and reduced vaso-occlusion after ATL146e treatment. (G-H) NY1DD mice, but not NY1DD x A2AR−/− mice, had decreased vascular permeability and increased oxygen saturation after ATL146e treatment. (I-J) NY1DD mice, but not NY1DD x A2AR−/− mice, displayed improved breathing parameters after ATL146e treatment. Data were analyzed by 1-way ANOVA with Neuman-Keuls posttesting; *P < .05. SO2: arterial oxygen saturation.

ATL146e treatment decreases pulmonary dysfunction in NY1DD mice by activation of the A2AR. C57BL/6, NY1DD, or NY1DD x A2AR−/− mice were treated with ATL146e (10 ng/kg/minute, 3 days) or vehicle (saline, 0.2% DMSO). (A-F) Lung sections from NY1DD mice, but not NY1DD x A2AR−/− mice have reduced alveolar thickening and reduced vaso-occlusion after ATL146e treatment. (G-H) NY1DD mice, but not NY1DD x A2AR−/− mice, had decreased vascular permeability and increased oxygen saturation after ATL146e treatment. (I-J) NY1DD mice, but not NY1DD x A2AR−/− mice, displayed improved breathing parameters after ATL146e treatment. Data were analyzed by 1-way ANOVA with Neuman-Keuls posttesting; *P < .05. SO2: arterial oxygen saturation.

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