부산대학교 도서관

We have previously reported that the prolonged transient acidosis during early reperfusion mediates the cardioprotective effects in canine hearts. Recently, postconditioning has been shown to be one of the novel strategies to mediate cardioprotection. We tested the contribution of the prolonged transient acidosis to the cardioprotection of postconditioning. Open-chest anesthetized dogs subjected to 90-min occlusion of the left anterior descending coronary artery and 6-h repeffusion were divided into four groups: 1) control group; no intervention after repeffusion (n = 6); 2) postconditioning (Postcon) group; four cycles of l-rain reperfusion and 1-min reocclusion (n = 7); 3) Postcon + sodium bicarbonate (NaHC[O.sub.3]) group; four cycles of 1-min reperfusion and 1-min reocclusion with the administration of NaHC[O.sub.3] (n = 8); and 4) NaHC[O.sub.3] group; administration of NaHC[O.sub.3] without postconditioning (n = 6). Infarct size, the area at risk (AAR), collateral blood flow during ischemia, and pH in coronary venous blood were measured. The phosphorylation of Akt and extracellular signal-regulated kinase (ERK) in ischemic myocardium was assessed by Western blot analysis. Systemic hemodynamic parameters, AAR, and collateral blood flow were not different among the four groups. Postconditioning induced prolonged transient acidosis during the early reperfusion phase. Administration of NaHC[O.sub.3] completely abolished the infarct size-limiting effects of postconditioning. Furthermore, the phosphorylation of Akt and ERK in ischemic myocardium induced by postconditioning was also blunted by the cotreatment of NaHC[O.sub.3]. In conclusion, postconditioning mediates its cardioprotective effects possibly via prolonged transient acidosis during the early reperfusion phase with the activation of Akt and ERK. acidosis; reperfusion; postconditioning; reperfusion injury salvage kinase