Abstract
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 α-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 effluent 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 μ/kg i.p.), as α-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 α-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 α-1-AR activation involved in cardioprotective effect of RAPC-mediated trough opening of KATP channels.
Highlights
Coronary artery disease represents a global burden on health care resources, and it is the leading cause of morbidity and mortality in the world by 2020.[1]
Effect of remote aortic preconditioning on ischemia and reperfusion-induced myocardial injury
Global ischemia for 30 min followed by reperfusion for 120 min significantly increased myocardial infarct size, release of lactate dehydrogenase (LDH), and CK-MB in coronary effluent (P < 0.05)
Summary
Coronary artery disease represents a global burden on health care resources, and it is the leading cause of morbidity and mortality in the world by 2020.[1] Repeated short episodes of ischemia and reperfusion have been demonstrated to make myocardium transiently more resistant to deleterious effects of prolonged ischemia and this paradoxical form of myocardial adaptation has been termed as ischemic preconditioning.[2] The occlusion of circumflex artery has produced protection of myocardium supplied by left anterior descending coronary artery and this phenomenon is termed as intracardiac preconditioning.[3] Short occlusion of renal[4] abdominal aorta or mesenteric artery[5] has been documented to prevent myocardium against ischemia and reperfusion-induced injury This phenomenon has been termed as “remote preconditioning” or intraorgan preconditioning or preconditioning at distant site.[6,7] RAPC is well-documented in various animal models, but the molecular mechanism involved in remote preconditioning is still not well defined.
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