Intra-cardiac remote ischemic post-conditioning attenuates ischemia-reperfusion injury in rats

Objectives. It remains unknown whether brief occlusion and relaxation of remote non-infarct-related coronary arteries limits infarct size. We tested the hypothesis that repetitive, brief, non-infarcting ischemia in one remote myocardial region, applied before sustained reperfusion to another intra-cardiac vasculature following infarcting ischemia, attenuates ischemia-reperfusion injury. Design. In anesthetized open-chest rats, the left main coronary artery (LCA) was occluded for 30 min followed by sustained relaxation for 120 min. All rats were randomly allocated to six groups (n=8): Control: without other interventions; Intra-cardiac remote ischemic post-conditioning (R-Post): before LCA relaxation, 3 cycles of 10 s ischemia by occluding the circumflex branch and 10 s reperfusion by relaxing it were applied; Atractyloside (Atr): given intravenously with atractyloside, an opener of the mitochondrial permeability transition pore; R-Post + Atr; Classical ischemic post-conditioning (Post): 3 cycles of 10 s reperfusion followed by 10 s ischemia were applied before 120 min of LCA relaxation; Sham: without LCA occlusion. We evaluated infarct size, cardiac function, cardiomyocyte ultrastructure and inflammatory processes. Results. Compared with Control, at the end of sustained reperfusion, R-Post and Post had smaller infarcts (respectively, 49%±5% vs. 32%±6% and 26%±5%, p