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Updated: Apr 17, 2026
Acute Myocardial Infarction in Rats
Published on: February 16, 2011
Remifentanil postconditioning has cross talk with adenosine receptors in the ischemic-reperfused rat heart
Jeon-Yu Ha1, Yong-Cheol Lee2, Sang-Jin Park3
1Department of Anesthesiology and Pain Medicine, Graduate School, Keimyung University, Daegu, Korea.
Background:
Although there is a possibility of cross talk between opioid and adenosine signaling pathways in the ischemic-reperfused myocardium, it is not clear that an ultra-short-acting opioid receptor agonist remifentanil-induced postconditioning (RPostC) has cross talk with adenosine receptor (ADR). The purpose of this study was to determine whether there is cross talk with ADR in RPostC.
Materials And Methods:
Isolated rat hearts were subjected to 30 min of regional ischemia and 2 h of reperfusion. RPostC was induced by 100 ng/mL of remifentanil perfusion, 5 min before reperfusion, followed by 5 min of reperfusion. The nonspecific opioid receptor antagonist naloxone (NAL) and the nonspecific ADR antagonist 8-(p-sulfophenyl) theophylline hydrate (8-SPT) were perfused for a 20-min period, 10 min before RPostC to the end of RPostC. Western blot analysis was performed to detect phospho-ERK1/2 in cultured cardiomyocytes.
Results:
In cultured cardiomyocytes, remifentanil incubation significantly increased the phosphorylation of ERK1/2 and this effect was blocked by both NAL and 8-SPT (P < 0.01 and P < 0.05, respectively). RPostC significantly reduced infarct size over ischemic area at risk from 34.1 ± 10.5% to 16.6 ± 7.5% (P < 0.05 versus control). The infarct-limitation effect of RPostC was reversed by both NAL (33.8 ± 13.0%, P < 0.05) and 8-SPT (35.7 ± 14.5%, P < 0.01).
Conclusions:
This study strongly implies that the intracellular signaling pathways of cardioprotection by RPostC has cross talk with ADR in the ischemic-reperfused myocardium.
