Fig. 5. Adora2b signaling in polymorphonuclear leukocyte (PMN)-depleted mice. Wild-type mice were treated with a monoclonal antibody directed against the granulocyte receptor 1 (GR-1) exclusively expressed on polymorphonuclear leukocytes (PMNs) 24 h before the experiment. GR-1 treatment decreased PMNs in peripheral blood from 2,500 ± 150 PMNs/μl (control) to 150 ± 75 PMNs (mean ± SD, n = 4 per group) (A ). Infarct sizes (ISs) are presented as percentage of the area at risk (AAR). The pretreatment with a PMN-depleting antibody alone led to ISs of 28 ± 8%. Additional administration of BAY 60-6583 during reperfusion in the presence of PMNs led to ISs of 24 ± 5%, and to 36 ± 2% in the absence of PMNs (B ). Measurement of serum troponin I concentrations by enzyme-linked immunosorbent assay (ELISA). Treatment with BAY 60-6583 during reperfusion resulted in troponin I values of 10 ± 4 ng/ml. GR-1 antibody treatment resulted in troponin I values of 12 ± 6 ng/ml. PMN depletion and subsequent BAY 60-6583 administration in the reperfusion resulted in troponin I values of 9 ± 4 ng/ml (C ). ISs were measured by double staining with Evans blue and triphenyltetrazolium chloride. ISs are expressed as the percentage of the AAR that underwent infarction. Representative images of ISs from the experiments in B and C are displayed (mean ± SD; n = 5 per group) (D ).