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Purpose: To elucidate the basis for the cardioprotective effect of dexmedetomidine pre-treatment on ROS-induced myocardial ischemia-reperfusion injury (IRI) in rats.
Methods: Sixty Sprague-Dawley (SD) rats were assigned to sham, model and dexmedetomidine intervention groups, each having 20 rats. Myocardial IRI was induced in the model and dexmedetomidine intervention groups using modified suture method. In sham group, chests of rats were opened, but without ligation, while dexmedetomidine intervention group was pre-treated with dexmedetomidine (5 μg/kg) before establishment of the IRI model. Protein expressions of adenosine 5‘-
monophosphate (AMP)-activated protein kinase (AMPK) was determined by Western blot assay. Mean fluorescence intensity of ROS was measured using flow cytometry.
Results: AMPK protein was significantly down-regulated in model rats, relative to sham rats, but significantly higher in dexmedetomidine intervention rats (p < 0.05). In model rats, mean ROS fluorescence intensity and degree of apoptosis of cardiomyocytes were higher than the corresponding values in sham rats (p < 0.05), but lower in dexmedetomidine intervention group.
Conclusion: Dexmedetomidine reduces oxidative stress in myocardial tissue and exerts a protective role by activating AMPK pathway and inhibiting mitochondrial generation of ROS. Therefore, this compound might have a potential clinical role in the management of IRI.