ROLE OF ADENOSINE A1 RECEPTOR IN CARDIAC MITOCHONDRIAL FUNCTION AT EARLY REPERFUSION PHASE, IN A REMOTE ISCHEMIC PRECONDITIONING MODEL

CALABRÓ, VALERIA; TIMOTEO MARCHINI; RICARDO GELPI; GARCES, MARIANA; BIN, ELIANA P; HÖCHT, CHRISTIAN; PAEZ, DIAMELA T; DEL MAURO, JULIETA; PABLO EVELSON; DONATO, MARTIN

MAR DEL PALTA

Congreso; LXIII REUNION ANUAL DE LA SOCIEDAD ARGENTINA DE INVESTIGACION CLINICA; 2018

SAIC

Adenosine is involved in classic preconditioning in most species andacts especially through adenosine A1 and A3 receptors. The aim ofour study was to evaluate whether remote ischemic preconditioning(rIPC) activates A1 adenosine receptors and improves mitochondrialfunction, thereby reducing myocardial infarct size. Isolated rathearts were subjected to 30 min of global ischemia and 60 min ofreperfusion (I/R). In a second group, before isolation of the heart, arIPC protocol (3 cycles of hindlimb ischemia/reperfusion) was performed.The infarct size was measured with tetrazolium staining,and eNOS expression/phosphorylation and mitochondrial functionwere evaluated after ischemia at 10 and 60 min of reperfusion. Asexpected, rIPC significantly decreased the infarct size. This beneficialeffect was only abolished when DPCPX (A1 receptor blocker)and L-NAME (NO synthesis inhibitor) were administered during thereperfusion phase. At the early reperfusion phase, rIPC induced significanteNOS phosphorylation, which was abolished by the perfusionwith an A1 receptor blocker. I/R lead to impaired mitochondrialfunction, which was attenuated by rIPC and mediated by A1 adenosinereceptors. In conclusion, we demonstrated that rIPC limitsmyocardial infarct by activation of A1 adenosine receptor at earlyreperfusion in the isolated rat heart. Interestingly, rIPC appears toreduce myocardial infarct size by improving mitochondrial functionduring myocardial reperfusion.