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2016•Zhonghua mazuixue zazhiRequires access

Effect of oxycodone postconditioning on myocardial ischemia-reperfusion injury in rats

Peining Yang, Yufang Leng, Yuanmei Ye, Xiaoli Ma, Ting Wang

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Abstract

Objective To evaluate the effect of oxycodone postconditioning on myocardial ischemia-reperfusion (I/R) injury in rats. Methods Forty pathogen-free healthy adult male Sprague-Dawley rats, weighing 200-300 g, were randomly divided into 4 groups (n=10 each) using a random number table: sham operation group (group S), myocardial I/R group (group I), oxycodone postconditioning group (group O), and selective protein kinase C inhibitor chelerythrine group (group CH). Myocardial ischemia was induced by 30 min occlusion of the left anterior descending branch of the coronary artery, followed by 120 min reperfusion.In group S, the left anterior descending branch of the coronary artery was only exposed but not ligated.In group CH, chelerythrine 5 mg/kg was injected intravenously and slowly via the jugular vein before ligation which was performed immediately after administration.In O and CH groups, oxycodone 0.5 mg/kg was injected intravenously and slowly via the jugular vein at 2 min before reperfusion.Arterial blood samples were taken at 120 min of reperfusion to detect the levels of cardiac troponin I (cTnI) and creatine kinase-MB (CK-MB) in serum.The hearts were removed after the animals were sacrificed to measure the myocardial infarct size by TTC staining. Results Compared with group S, the levels of cTnI and CK-MB in serum and myocardial infarct size were significantly increased in I, O and CH groups (P<0.05). Compared with group I, the levels of cTnI and CK-MB in serum and myocardial infarct size were significantly decreased in O and CH groups (P<0.05). Compared with group O, the levels of cTnI and CK-MB in serum and myocardial infarct size were significantly increased in group CH (P<0.05). Conclusion Oxycodone postconditioning can mitigate myocardial I/R injury in rats, and the mechanism is partially related to activation of protein kinase C signaling pathway. Key words: Oxycodone; Ischemic postconditioning; Myocardial reperfusion injury; Protein kinase C

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Objective To evaluate the effect of oxycodone postconditioning on myocardial ischemia-reperfusion (I/R) injury in rats. Methods Forty pathogen-free healthy adult male Sprague-Dawley rats, weighing 200-300 g, were randomly divided into 4 groups (n=10 each) using a random number table: sham operation group (group S), myocardial I/R group (group I), oxycodone postconditioning group (group O), and selective protein kinase C inhibitor chelerythrine group (group CH). Myocardial ischemia was induced by 30 min occlusion of the left anterior descending branch of the coronary artery, followed by 120 min reperfusion.In group S, the left anterior descending branch of the coronary artery was only exposed but not ligated.In group CH, chelerythrine 5 mg/kg was injected intravenously and slowly via the jugular vein before ligation which was performed immediately after administration.In O and CH groups, oxycodone 0.5 mg/kg was injected intravenously and slowly via the jugular vein at 2 min before reperfusion.Arterial blood samples were taken at 120 min of reperfusion to detect the levels of cardiac troponin I (cTnI) and creatine kinase-MB (CK-MB) in serum.The hearts were removed after the animals were sacrificed to measure the myocardial infarct size by TTC staining. Results Compared with group S, the levels of cTnI and CK-MB in serum and myocardial infarct size were significantly increased in I, O and CH groups (P<0.05). Compared with group I, the levels of cTnI and CK-MB in serum and myocardial infarct size were significantly decreased in O and CH groups (P<0.05). Compared with group O, the levels of cTnI and CK-MB in serum and myocardial infarct size were significantly increased in group CH (P<0.05). Conclusion Oxycodone postconditioning can mitigate myocardial I/R injury in rats, and the mechanism is partially related to activation of protein kinase C signaling pathway. Key words: Oxycodone; Ischemic postconditioning; Myocardial reperfusion injury; Protein kinase C

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Available abstract

Objective To evaluate the effect of oxycodone postconditioning on myocardial ischemia-reperfusion (I/R) injury in rats. Methods Forty pathogen-free healthy adult male Sprague-Dawley rats, weighing 200-300 g, were randomly divided into 4 groups (n=10 each) using a random number table: sham operation group (group S), myocardial I/R group (group I), oxycodone postconditioning group (group O), and selective protein kinase C inhibitor chelerythrine group (group CH). Myocardial ischemia was induced by 30 min occlusion of the left anterior descending branch of the coronary artery, followed by 120 min reperfusion.In group S, the left anterior descending branch of the coronary artery was only exposed but not ligated.In group CH, chelerythrine 5 mg/kg was injected intravenously and slowly via the jugular vein before ligation which was performed immediately after administration.In O and CH groups, oxycodone 0.5 mg/kg was injected intravenously and slowly via the jugular vein at 2 min before reperfusion.Arterial blood samples were taken at 120 min of reperfusion to detect the levels of cardiac troponin I (cTnI) and creatine kinase-MB (CK-MB) in serum.The hearts were removed after the animals were sacrificed to measure the myocardial infarct size by TTC staining. Results Compared with group S, the levels of cTnI and CK-MB in serum and myocardial infarct size were significantly increased in I, O and CH groups (P<0.05). Compared with group I, the levels of cTnI and CK-MB in serum and myocardial infarct size were significantly decreased in O and CH groups (P<0.05). Compared with group O, the levels of cTnI and CK-MB in serum and myocardial infarct size were significantly increased in group CH (P<0.05). Conclusion Oxycodone postconditioning can mitigate myocardial I/R injury in rats, and the mechanism is partially related to activation of protein kinase C signaling pathway. Key words: Oxycodone; Ischemic postconditioning; Myocardial reperfusion injury; Protein kinase C

Key concepts: Troponin I, Medicine, Chelerythrine, Myocardial infarction, Anesthesia, Creatine kinase, Reperfusion injury, Internal medicine

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Effect of oxycodone postconditioning on myocardial ischemia-reperfusion injury in rats — Research Paper | ScholarLens