Journal List > Korean Circ J > v.26(5) > 1073215

Kim, Shin, Park, Choi, and Shim: The Role of the Adenosine Receptor Subtypes and Protein Kinase C in Ischemic Preconditioning in the in Vivo Cat Heart

Abstract

Background

It is well known that ischemic preconditioning protects the heart against infarction or arrhythmias from a subsequent ischemic injury. Recent laboratory data indicate that the adenosine during the ischemic period may trigger protection via A1 or A3 adenosine receptor and also protein kinase C(PKC) plays a central role. This study was designed to determine the role of adenosine receptor subtypes and PKC in the preconditioning protection.

Methods

All cat heart groups were subjected to 40min ischemia and 30min reperfusion. The preconditioning protocol consists of 4min ischemia and then 10min of reperfusion 4 times. The effects of ischemic preconditioning, nonselective adenosine receptor blocker(SPT), an A1 specific antagonist(DPCPX) and protein kinase C inhibitor(Polymyxin B), on ischemic preconditioning were determined by infarction size. There were 5 groups : (1) control group (Group 1, n=10)(2) Ischemic preconditioned group(Group 2, n=9)(3) DPCPX pretreatment group(Group 3, n=6)(4) SPT preteatment group(Group 3, n=6)(5) Polymyxin B pretreatment group(Group 5, n=6). SPT and DPCPX were given intravenously 5 min before ischemic preconditioning. Polymyxin B was administered to cats for 30min during ischemic preconditioning period.

Results

Ischemic preconditioning only or pretreatment with DPCPX prior to preconditioning demonstrated a significant reduction in infarct size(22.6±1.5, 25.4±0.9% infarction of the risk zone, respectively, p<0.05) with respect to control, SPT-pretreatment, and polymyxin B-pretreatment groups(44.0±1.7, 43.0±2.0 and 40.3±0.4% infarction of the risk zone, respectively).

Conclusion

Ischemic preconditioning protects heart from subsequent ischemia. Protection was blocked by SPT and protein kinase C inhibitor(polymyxin B), but not by A1 antagonist DPCPX. The cardioprotective effects by ischemic preconditioning in the in vivo cat heart appear to be dependent on A3 adenosine receptors and activation of protein kinase C.

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