Abstract
Purpose: To study the effect of dexmedetomidine on myocardial ischemia-reperfusion injury (MI/RI)- induced imbalance on oxidant-prooxidant status and apoptotic changes in rats.
 Methods: Ninety (90) male Wistar rats were randomly divided into three groups – sham, model and post-treatment. In model rats, the anterior descending branch of the left coronary artery was ligated for 25 min, prior to their being subjected to reperfusion for 2 h. Rats in the post-treatment group were subjected to ligation at the anterior descending branch of the left coronary artery for 25 min, but they were intravenously injected with dexmedetomidine at a dose of 10 μg/kg prior to reperfusion. There was no ligation in the sham group. Malondialdehyde (MDA), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were assayed. Lactate dehydrogenase (LDH) and creatine kinase isoenzyme (CK-MB) levels were also evaluated. Apoptosis was measured with TdT-mediated dUTP nick end labeling (TUNEL) assay.
 Results: Compared with the sham group, MDA level in the model group was significantly rose, while SOD and GSH-Px activities were markedly decreased (p < 0.05). Moreover, there were higher LDH and CK-MB activities in model rats than in the sham rats, but they were significantly lower in the posttreatment group than in the model group (p < 0.05). Apoptosis was higher in model rats than in sham operation rats, but was markedly decreased in post-treatment rats than in model rats (p < 0.05).
 Conclusion: Post-treatment with dexmedetomidine exerts myocardial protective effect via significant reduction in oxidative stress-induced myocardial injury and apoptosis.
 Keywords: Dexmedetomidine, Myocardial ischemia-reperfusion injury, Antioxidant status, Programmed cell death
Highlights
Coronary atherosclerotic heart disease constitutes a serious threat to human life and health
It is known that myocardial ischemia-reperfusion injury (MI/RI) is serious pathophysiological change in myocardial tissue caused by the restoration of blood supply, which results in severe myocardial injury, irreversible damage, and even myocardial death [3]
It has been found that dexmedetomidine pre-treatment exerts protective effects on myocardium, but very little is known about the effect of dexmedetomidine pretreatment on the myocardium [6]
Summary
Coronary atherosclerotic heart disease constitutes a serious threat to human life and health. The others were GSH-Px assay kit (Shanghai Suobao Biotechnology Co. Ltd., specification: 50T); LDH assay kit (DOJINDO Laboratories, specification: 100T); CK-MB assay kit (Shanghai Yiyan Biotechnology Co. Ltd., specification: 96T); TUNEL apoptosis analysis kit (Beijing Baiaolaibo Technology Co. Ltd., specification: 50T), and dexmedetomidine (Jiangsu Hengrui Pharmaceutical Co. Ltd., production batch number: 20170248, specification: 2 mL: 200 g). The anterior descending branch of the left coronary artery was ligated for 25 min, and the rats were subjected to reperfusion for 2 h. Rats in the posttreatment group were ligated in the anterior descending branch of the left coronary artery for 25 min, but were intravenously injected with dexmedetomidine at a dose of 10 μg/kg prior to reperfusion. Apoptosis in rats in each group was measured using TUNEL assay. Values of p < 0.05 were taken as indicative of statistical significance difference
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