Adenosine inhibition of neutrophil damage during reperfusion does not involve KATP-channel activation

1 Department of Cardiothoracic Surgery, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North Carolina 27157-1096; and 2 Department of Emergency Medicine, Jefferson Medical College, Philadelphia, Pennsylvania 19107 This study tests the hypothesis that cardioprotection exerted by adenosine A 2 -receptor activation and neutrophil-related events involves stimulation of ATP-sensitive potassium (K ATP ) channels on neutrophils during reperfusion. The adenosine A 2 agonist CGS-21680 (CGS) inhibited superoxide radical generation from isolated rabbit polymorphonuclear neutrophils (PMNs) in a dose-dependent manner from 17.7 ± 2.1 to 7.4 ± 1.3 nmol/5 × 10 6 PMNs ( P