Objective：This study aims to evaluate the role of poly（ADP-ribose）polymerase-1（PARP-1）in attenuation of myocardial ischemia-reperfusion injury treated by dexmedetomidine in rats. Methods：Forty eight healthy male Sprague Dawley rats，8~12 weeks old，weighing 200~240 g were selected. The rats were then randomly divided into 3 groups（n=16）：Sham operation group（S group），lung ischemia-reperfusion group（I/R group）and I/R+dexmedetomidine group（I/R+Dex group）. In S group，the anterior descending branch was only exposed but not ligated；Myocardial I/R was induced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 120 min of reperfusion in I/R group and I/R+Dex group. Dexmedetomidine 5 μg/kg were injected intraperitoneally 15 min before reperfusion in I/R+Dex group while physiological saline was injected in S and I/R groups. The mean arterial pressure（MAP），heart rate（HR）and heart rate systolic blood pressure product（RPP）were observe and recorded before ischemia（T0），30 min of ischemia（T1） and reperfusion of 60 min（T2） and 120 min reperfusion（T3）. At the end of 120 min reperfusion，hearts were removed for determination of the myocardial infarct size in the left ventricular myocardial tissues. The expression of PARP-1 activity markers（PAR）and apoptosis related protein Caspase-3 in myocardial tissue were investigated by Western blot. TNF-a and IL-6 levels were examined by ELISA. Results：Compared with the time point of T0，the MAP，HR and RPP were significantly decreased at time point of T1-T3 in I/R group and I/R+Dex group（P＜0.05）. Compared with S group，MAP，HR and RPP were significantly decreased at time point of T1-T3，myocardial infarct size，TNF-a and IL-6 levels，PAR and Caspase-3 expressions were increased in I/R group and I/R+Dex group（P＜0.05）. Compared with I/R group，MAP，HR and RPP were significantly decreased at time point of T1-T2 while increased at T3，myocardial infarct size，TNF-a and IL-6 levels，PAR and Caspase-3 expressions were decreased in I/R+Dex group（P＜0.05）. Conclusion：Dexmedetomidine can attenuate myocardial ischemia-reperfusion injury．The mechanism may be associated with reducing the activation of PARP-1，and then inhibit inflammation and apoptosis in myocardial tissue.