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Am J Physiol Heart Circ Physiol 292: H2004-H2008, 2007. First published January 5, 2007; doi:10.1152/ajpheart.01051.2006
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Prolonged transient acidosis during early reperfusion contributes to the cardioprotective effects of postconditioning

¹Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Suita; ²Cardiovascular Division of Medicine, National Cardiovascular Center of Japan, Suita; ³Cardiovascular Division, Osaka Police Hospital, Osaka; ⁴Department of Bioregulatory Medicine, Osaka University Graduate School of Medicine, Suita; and ⁵Department of Physiological Science, Tokai University School of Medicine, Isehara, Japan

Submitted 25 September 2006 ; accepted in final form 18 December 2006

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 reperfusion were divided into four groups: 1) control group; no intervention after reperfusion (n = 6); 2) postconditioning (Postcon) group; four cycles of 1-min reperfusion and 1-min reocclusion (n = 7); 3) Postcon + sodium bicarbonate (NaHCO₃) group; four cycles of 1-min reperfusion and 1-min reocclusion with the administration of NaHCO₃ (n = 8); and 4) NaHCO₃ group; administration of NaHCO₃ 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 NaHCO₃ 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 NaHCO₃. 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

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