Adenosine A_1 receptors and mitochondria: targets of remote ischemic preconditioning

摘要

Adenosine is involved in classic preconditioning in most species and acts especially through adenosine Ai and A3 receptors. The aim of the present study was to evaluate whether remote ischemic preconditioning (rIPC) activates adenosine Ai receptors and improves mitochondria function, thereby reducing myocardial infarct size. Isolated rat hearts were subjected to 30 min of global ischemia and 60 min of reperfusion ischemia-reperfusion (I/R). In a second group, before isolation of the heart, a rIPC protocol (3 cycles of hindlimb I/R) was performed. Infarct size was measured with tetra-zolium staining, and Akt/endothelial nitric oxide (NO) synlhase (eNOS) expression/phosphorylation and mitochondria function were evaluated after ischemia at 10 and 60 min of reperfusion. As expected, rIPC significantly decreased infarct size.