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• W2130162368 endingPage "320" @default.
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• W2130162368 abstract "Ischemic postconditioning (Post-C), brief cycles of myocardial ischemia and reperfusion during the early phase of reperfusion, is considered as a novel adjunct strategy to protect myocardium.However, the exact mechanism remains unclear and should be determined. Methods:The hearts of male Wistar rats were subjected to 30 min ischemia and 2 hrs reperfusion.Control rats had no intervention either before or after left coronary artery occlusion.Post-C was elicited by 6 cycles of 10s reperfusioninterspersed by 10s ischemia immediately after onset of reperfusion.Subsets of postconditioning rats were treated with drugs as followings; naloxone (non-selective opioid receptor antagonist), naltrindole (a δ-opioid receptor antagonist), SB216763 (a glycogen synthase kinase 3β inhibitor, GSK-3β inhibitor), or atractyloside (a mitochondrial permeability transition pore opener, mPTP opener). Results:Post-C significantly reduced infarct size (15.9 ± 2.4%, P = 0.003) compared to control (29.9 ± 3.7%).The anti-infarct effect by Post-C was blocked by both naloxone (25.5 ± 3.9%, P = 0.044) and naltrindole (26.9 ± 2.3%, P = 0.022).Infarct size limiting effect by Post-C was also abolished by atractyloside (30.6 ± 3.6%, P = 0.003).In SB216763 with naloxone treated animals, the infarct size was decreased (17.4 ± 3.2%, P = 0.007) but not in SB216763 with atractyloside treated animals (27.4 ± 2.6%) compared to control. Conclusions:These data suggest that Post-C may protect myocardium by inhibiting mPTP opening via δ-opioid receptor activation.GSK-3β is a downstream mediator of opioid receptors and an upstream mediator of mPTP opening in Post-C." @default.
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• W2130162368 date "2008-01-01" @default.
• W2130162368 modified "2023-10-17" @default.
• W2130162368 title "Ischemic Postconditioning Inhibits Mitochondrial Permeability Transition Pore via Opioid Receptor Activation in Intact Rat Heart" @default.
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• W2130162368 doi "https://doi.org/10.4097/kjae.2008.54.3.320" @default.
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