Role of ATP-sensitive K+ channels in oxycodone postconditioning-induced attenuation of myocardial ischemia-reperfusion injury in rats

Objective To evaluate the role of ATP-sensitive K+ channels (KATP channels) in oxycodone postconditioning-induced attenuation of myocardial ischemia-reperfusion (I/R) injury in rats. Methods Forty healthy adult male Sprague-Dawley rats, aged 8-12 weeks, weighing 200-300 g, were randomly divided into 4 groups (n=10 each) using a random number table: sham operation group (group S), group I/R, oxycodone postconditioning group (group OP), and KATP channel blocker glibenclamide plus oxycodone postconditioning group (group GOP). Myocardial I/R was produced by 30 min occlusion of the anterior descending branch of the left coronary artery followed by 120 min reperfusion.In group S, the anterior descending branch of the left coronary artery was only exposed but not ligated.In group GOP, glibenclamide 1 mg/kg was injected via the jugular vein before ischemia.In OP and GOP groups, oxycodone 0.5 mg/kg was injected via the jugular vein at 5 min prior to reperfusion, and the equal volume of normal saline was given in S and I/R groups.At 120 min of reperfusion, blood samples were collected from the carotid artery for determination of the level of serum cardiac troponin I (cTnI). The animals were then sacrificed, and the hearts were removed for determination of the myocardial infarct size in the left ventricle. Results Compared with group S, the concentration of serum cTnI and myocardial infarct size were significantly increased in I/R, OP and GOP groups (P<0.05). Compared with group I/R, the concentration of serum cTnI and myocardial infarct size were significantly decreased in OP and GOP groups (P<0.05). Compared with group OP, the concentration of serum cTnI and myocardial infarct size were significantly increased in group GOP (P<0.05). Conclusion KATP channel opening is involved in oxycodone postconditioning-induced attenuation of myocardial I/R injury in rats. Key words: KATP channels; Oxycodone; Ischemic postconditioning; Myocardial reperfusion injury