Neutrophil inhibition contributes to cardioprotection by postconditioning

Background Postconditioning (postcon) reduces infarct size, myocardial superoxide (•O2) generation, and neutrophil (PMN) accumulation. It is unknown whether inhibition of PMNs influence cardioprotection by postcon. The present study tested the following hypotheses: (1) myocardial salvage by postcon is modified by inhibition of PMNs and (2) postcon directly inhibits PMN •O2 generation. Methods For hypothesis 1, a deductive approach was used to determine infarct size in vivo with and without PMNs in rats, and for hypothesis 2, blood sampled from the anterior interventricular vein (AIV) in a canine model was used. Protocol 1: anesthetized rats, subjected to 30 min of coronary artery occlusion and 3 h of reperfusion, were randomized to control (n = 13), postcon (n = 13), PMN‐depletion: (n = 9), and postcon in PMN‐depleted rats (n = 9). Protocol 2: blood was sampled at baseline, 2 h and 24 h from the AIV, draining the area at risk (AAR) in anesthetized dogs with 60 min coronary occlusion ± postcon; whole blood was analyzed for •O2 by luminol‐enhanced chemiluminescence. Results Postcon and PMN depletion reduced infarct size (42.6 ± 2.1%, P