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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Postconditioning protects rabbit hearts through a protein kinase C-adenosine A(2b) receptor cascade.

OBJECTIVE: Ischemic postconditioning protects the reperfused heart from infarction, and this protection is dependent on the occupancy of adenosine receptors. We further explored the role of adenosine receptors in this salvage. METHODS: In situ rabbit hearts underwent 30min of regional ischemia and 3h of reperfusion, and postconditioning was effected with four cycles of 30-s reperfusion/30-s coronary artery occlusion at the end of ischemia. RESULTS: Postconditioning reduced infarct size from 40.2+/-3.4% of the risk zone in untreated hearts to 15.5+/-2.5%. Protection by postconditioning was blocked by either the non-selective adenosine receptor blocker 8-p-(sulfophenyl)theophylline or the A(2b)-selective antagonist MRS 1754, injected intravenously 5min before reperfusion. The protein kinase C (PKC) antagonist chelerythrine also aborted postconditioning's salvage, indicating a PKC-dependent mechanism. Neither the A(1)-selective antagonist 8-cyclopentyl-1,3-dipropylxanthine nor the A(2a)-selective antagonist 8-(13-chlorostyryl)caffeine had an effect on protection. The non-selective but A(2b)-potent adenosine agonist 5'-(N-ethylcarboxamido)adenosine (NECA) infused from 5min before to 1h after reperfusion mimicked postconditioning's effect on infarct size (17.2+/-2.7% infarction) and MRS 1754 blocked the NECA-induced cardioprotection, confirming that A(2b) activation was protective. The PKC activator phorbol 12-myristate 13-acetate delivered just before reperfusion also duplicated the protective effect of postconditioning (16.3+/-4.1% infarction), and co-administration of the PKC antagonist chelerythrine aborted PMA's protection, confirming that the protection was the result of PKC activation. NECA's protective effect was not affected by chelerythrine, but rather MRS 1754 blocked PMA's salutary effect (42.8+/-1.0% infarction), suggesting that the A(2b) receptor's effect is under control of PKC. Finally, wortmannin, a blocker of phosphatidylinositol 3-kinase, also abrogated protection by PMA. CONCLUSIONS: Salvage of ischemic myocardium by postconditioning is dependent on activation of A(2b) receptors, which in turn depends on activation of PKC. It is still unclear why PKC activation is required to make the heart's adenosine become protective.[1]


  1. Postconditioning protects rabbit hearts through a protein kinase C-adenosine A(2b) receptor cascade. Philipp, S., Yang, X.M., Cui, L., Davis, A.M., Downey, J.M., Cohen, M.V. Cardiovasc. Res. (2006) [Pubmed]
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