Background: Remote preconditioning is a phenomenon in which brief episodes of ischemia and reperfusion to remote organs protect the target organ against sustained ischemia/reperfusion (I/R)-induced injury. Protective effects of remote aortic preconditioning (RAPC) are well established in the heart, but their mechanisms still remain to be elucidated. Objective: This study has been designed to investigate the possible involvement of ∝-1-adrenergic receptor (AR) and KATP channels in cardio-protective effect of RAPC in isolated rat heart. Materials and Methods: Four episodes of ischemia and reperfusion, each comprising of 5 min occlusion and 5 min reperfusion, were used to produce RAPC. Isolated perfused rat heart was subjected to global ischemia for 30 min followed by reperfusion for 120 min. Coronary effl uent was analyzed for LDH and CK-MB release to assess the degree of cardiac injury. Myocardial infarct size was estimated macroscopically using TTC staining. Results: Phenylephrine (20 ∝g/kg i.p.), as ∝-1-AR agonist, was noted to produce RAPC-like cardio-protection. However, administration of glibenclamide concomitantly or prior to phenylephrine abolished cardioprotection. Moreover, prazocin (1 mg/kg. i.p), as ∝-1-AR antagonist and glibenclamide (1 mg/kg i.p), a KATP channel blocker, abolished the cardioprotective effect of RAPC. Conclusion: These data provide the evidence that ∝-1-AR activation involved in cardioprotective effect of RAPC-mediated trough opening of KATP channels.
Key words: Cardio-protection, ischemic preconditioning, ischemia / reperfusion injury, remote aortic preconditioning.