Effect of pressure overload on cardioprotection of postconditioning: comparison to pressure unloading

Abstract

This study tests the hypothesis that pressure overload attenuates cardioprotective effect of postconditioning. Accordingly, following stabilization, Langendorff‐perfused hearts of male rats were subjected to regional ischemia (I; 40 min) followed by reperfusion (R; 2 hrs) with perfusion pressure set at either 80 or 160 cmH2O. Postconditioning was induced by six cycles of I and R (10 sec. each) immediately at the end of index I followed by continuous R (n=7‐10 hearts/condition). Comparisons were made to pressure unloading which consisted of perfusion of heats at 160 cmH2O during the stabilization and I periods followed by switchover to 80 cmH2O during R (n=6 hearts). Elevation in perfusion pressure resulted in larger infarcts (p<0.05). Postconditioning reduced infarct size at either pressure (p<0.05); nonetheless, a significant differential persisted between hearts perfused at the high and low perfusion pressures. Interestingly, pressure unloading markedly reduced infarct size, an effect more prominent than that conferred by postconditioning. The results provide evidence for the deleterious impact of pressure overload on postconditioning‐induced cardioprotection. Further, the marked cardioprotective effect of pressure unloading suggests involvement of cardioprotective pathways that may be distinct from those mobilized by postconditioning. Supported by AHA, Southeast Affiliate.