Figure 1.
Figure 1. Influence of adenosine receptor inhibition on PMN adhesion to posthypoxic endothelia. HMEC-1s were subjected to normoxia (pO2 147 mm Hg for 48 h, □) or hypoxia (pO2 20 mm Hg for 48 h, ▪) followed by determination of FMLP-stimulated PMN adhesion in the presence or absence of indicated concentrations of adenosine receptor antagonists. PMN adhesion was determined by assessment of BCECF-labeled PMNs binding to normoxic or posthypoxic HMEC-1s. Results are presented as the fold change (± SD) in BCECF fluorescence in the presence of (A) the nonselective antagonist 8-phenyl-theophylline (8-PT); (B) the AdoRA1 antagonist DPCPX; (C) the AdoRA2A antagonist ZM 241385; (D) the AdoRA2A antagonist CSC; (E) the AdoRA2B antagonist MRS 1754; (F) or the AdoRA3 antagonist MRS 1334. Results are presented as the fold change (± SD) in BCECF fluorescence (μM concentrations; *P < .05 compared with normoxia; #P < .025 compared with no antagonist control).

Influence of adenosine receptor inhibition on PMN adhesion to posthypoxic endothelia. HMEC-1s were subjected to normoxia (pO2 147 mm Hg for 48 h, □) or hypoxia (pO2 20 mm Hg for 48 h, ▪) followed by determination of FMLP-stimulated PMN adhesion in the presence or absence of indicated concentrations of adenosine receptor antagonists. PMN adhesion was determined by assessment of BCECF-labeled PMNs binding to normoxic or posthypoxic HMEC-1s. Results are presented as the fold change (± SD) in BCECF fluorescence in the presence of (A) the nonselective antagonist 8-phenyl-theophylline (8-PT); (B) the AdoRA1 antagonist DPCPX; (C) the AdoRA2A antagonist ZM 241385; (D) the AdoRA2A antagonist CSC; (E) the AdoRA2B antagonist MRS 1754; (F) or the AdoRA3 antagonist MRS 1334. Results are presented as the fold change (± SD) in BCECF fluorescence (μM concentrations; *P < .05 compared with normoxia; #P < .025 compared with no antagonist control).

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