Abstract
Introduction The role of polymorphonuclear neutrophils (PMN) in myocardial ischemia and reperfusion (I/R) is controversially discussed. The PMN surface protein CD11b/CD18 plays a critical role for PMN activation and adhesion. Using CD11b/CD18 deficient (CD11b-/-) mice we herein sought to further elucidate the effects of infiltrating PMN on ventricular remodeling and arrhythmogenesis in the context of myocardial I/R. Methods and Results Wildtype (WT) and CD11b-deficient (CD11b-/-) mice of C57BL/6J background were subjected to 40 minutes of myocardial ischemia by ligation of the left anterior descending artery following 6- or 48 hours of reperfusion (I/R). CD11b-/- resulted in significantly less myocardial myeloperoxidase release (MPO+ cells / field of view: WT: 308.4 ± 22.2 vs. CD11b-/-: 178.3 ± 13.1, p Conclusions Decreased myocardial PMN infiltration and oxidative protein modifactions caused by the absence of CD11b/CD18 suggests a clear role of PMN infiltration for maldadaptive left ventricular remodelling and arrhythmogenesis following myocardial I/R.
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