Background: It is known that brief episode(s) of ischemia/reperfusion applied prior or after myocardial ischemia to peripheral tissue located at a distance from the heart significantly reduce myocardial infarct size. This phenomenon is called remote ischemic conditioning (RIc). Objective: The aim was compared the efficacy of RIc in
protecting the heart when the RIc stimulus is applied prior to myocardial ischemia (remote ischemic preconditioning; rIPC), or at the onset of myocardial reperfusion (remote ischemic postconditioning; rIPost). Methods: In order to induce myocardial infarction, we used mice (FVB, 24 g) which were subjected to 30 min of left coronary artery occlusion followed by 120 min of reperfusion. rIPC and rIPost were induced by 3 cycles of 5 min of ischemia followed by 5 min of reperfusion of the left femoral artery. The infarct size was measured using Evans blue (Risk Area) and Triphenyltetrazolium chloride (Infarct size). Results: The ischemia/reperfusion protocol (30 min of ischemia and 120 min of reperfusion) induced an infarct size of 69.13±3.22 %. The rIPC and rIPost significantly reduced infarct size to 51.17±4.36 (p<0.05) and 33.33±4.10 % (p< 0.05), respectively. Bilateral vagotomy completely abolished cardioprotection induced by rIPC but not by rIPost. Both the femoral vein occlusion (FVO) and the administration of DPCPX (A1 adenosine receptor blocker) abolished the beneficial effect of rIPost. Conclusions: These results indicate that RIc confers potent cardioprotection when is applied before myocardial ischemia or at the onset of myocardial reperfusion. Cardioprotection by rIPC is critically dependent on
parasympathetic efferent innervation (vagal nerve), while rIPost appears to rely on a different signaling pathway(s) that involved the A1 adenosine receptor activation.