Abstract
Objective To evaluate the role of phosphatidylinositol 3-kinase (PI3K)/protein-serinethreonine kinases (Akt) signaling pathway in dexmedetomidine postconditioning-induced reduction of myocardial ischemia-reperfusion (I/R) injury in rats.Methods Seventy-two healthy male Sprague-Dawley rats,aged 4-5 months,weighing 200-240 g,were heparinized and anesthetized with intraperitoneal pentobarbital sodium 40 mg/kg.Their hearts were rapidly excised and perfused in a Langendorff apparatus with oxygenated (95％ O2-5％ CO2) K-H solution at 0-4℃.The isolated hearts were randomly divided into 6 groups (n =12 each):control group (group C),group I/R,dexmedetomidine postconditioning group (gruop D),solvent group (group DMSO),PI3K inhibitor LY294002 group (group L) and LY294002 + dexmedetomidine postconditioning group (group L + D).After a 20 min stabilization period,the hearts were continuously perfused with K-H solution for 120 min in group C and were subjected to 30 min of global no-flow ischemia followed by 90 min of repeffusion in the other groups.Dexmedetomidine 100 nmo/L was added during the initial 30 min of reperfusion in D and L + D groups.LY294002 15 μmol/L was added in L group.0.02％ DMSO containing 15 μmol/L LY294002 was added in L + D group.0.02％ DMSO was added in DMSO group.HR,left ventricular end-diastolic pressure,left ventricular developed pressure and ± dp/dtmax were recorded at the end of 20 min stabilization and 15,30 and 90 min of reperfusion.The expression of phosphorylated Akt (p-Akt) and Akt was measured at 30 min of reperfusion.Myoeardial infarct size was determined using TTC staining at 90 min of reperfusion.Results Compared with group C,HR,left ventricular developed pressure and ± dp/dtmax were significantly decreased,and left ventricular enddiastolic pressure and myocardial infarct size were increased in the other 5 groups,and the expression of p-Akt was significantly up-regulated in group D (P ＜ 0.05).Compared with group I/R,HR was significantly decreased at 15 and 30 min of reperfusion,the expression of p-Akt was up-regulated,and myocardial infarct size was decreased in group D (P ＜ 0.05).Compared with group D,the expression of p-Akt was down-regulated,and myocardial infarct size and HR was increased in L + D group (P ＜ 0.05).Conclusion Dexmedetomidine postconditioning attenuates myocardial I/R injury throuth activating PI3K/Akt signaling pathway in rats. Key words: 1-PhosphatidyIinositol 3-kinase ; Protein-serine-threonine kinases ; Dexmedetomidine ; Myocardial reperfusion injury; Postconditioning
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