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KMID : 0356920100580020162
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Korean Journal of Anesthesiology
2010 Volume.58 No. 2 p.162 ~ p.168
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Cardioprotection by kappa-opioid receptor agonist U50488H is mediated by opioidergic regulation but not by calcium current modulation
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Chun Kook-Jin
Jang Young-Ho
Kim June-Hong
Kim Jun
Park Yong-Hyun
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Abstract
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Background: Because the κ-opioid receptor (OR) agonist U50488H stimulates opioidergic regulation and inhibits L-type Ca2+ channels, this study was aimed at assessing the roles of OR and L-type Ca2+ channels on U50488H-induced cardioprotection.
Methods: Langendorff-perfused rat hearts were subjected to 30 min of regional ischemia and 2 h of reperfusion. Isolated hearts were treated with U50488H with or without the κ-OR antagonist nor-binaltorphimine (nor-BNI) or the Ca2+ channels activator BAY K 8644. Infarct size was measured with 2,3,5-triphenyltetrazolium chloride staining.
Results: U50488H treatment at reperfusion: (1) significantly reduced infarct size (11.3 ± 1.3%) compared to control hearts (27.7 ± 1.1%, P < 0.001), an effect that was completely blocked by nor-BNI (24.0 ± 0.9%, P < 0.001 vs. U50488H) but not by BAY K 8644 (7.1 ± 1.7%, P > 0.05 vs. U50488H); (2) significantly increased left ventricular developed pressure (65.3 ± 4.8%) after 2 h of reperfusion compared to control hearts (44.8 ± 3.6%, P < 0.05), an effect that was abrogated by nor-BNI (40.5 ± 4.5%, P > 0.05 vs. control) but not by BAY K 8644 (64.3 ± 5.6%, P < 0.01 vs. control); and (3) significantly decreased heart rate (P < 0.01 vs. control), an effect that was completely abrogated by both nor-BNI and BAY K 8644.
Conclusions: U50488H significantly limits myocardial infarction and stunning in isolated rat hearts after ischemia-reperfusion induction. The infarct size limitation and contractility improvement observed with U50488H treatment during reperfusion are entirely mediated by OR stimulation and not by Ca2+ channel modulation.
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KEYWORD
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Coronary occlusion, Myocardial infarction, Opioid receptors, Reperfusion
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