右美托咪啶预处理对心肌缺血再灌注损伤的保护作用及钙循环调控蛋白的影响  被引量:3

Protective effects of dexmedetomidine preconditioning in rats with myocardial ischemia reperfusion injury and the effects on calcium regulatory proteins

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作  者:李霞[1,2] 彭碧文[1] 董航[2] 

机构地区:[1]武汉大学基础医学院,湖北武汉430000 [2]江汉大学附属医院麻醉科,湖北武汉430000

出  处:《海南医学》2015年第18期2668-2670,共3页Hainan Medical Journal

摘  要:目的观察右美托咪定预处理对心肌缺血再灌注损伤的保护作用及心肌细胞钙循环调控蛋白兰尼碱受体(Ry R2)和肌浆网钙泵(SERCA2a)的影响。方法 45只大鼠随机分为3组,假手术组(Sham组),缺血再灌注组(I/R组),右美托咪定预处理组(DEXM组)。DEXM组在缺血前2 h经腹腔注射右美托咪定100μg/kg。监测各组大鼠缺血30 min及再灌注120 min的血流动力学参数评估心功能,以伊文氏蓝-红四氮唑(TTC)染色法测定心肌梗死面积,以实时定量PCR法检测心肌组织Ry R2和SERCA2a的m RNA表达水平。结果 I/R组心肌梗死面积(41.5±2.9)%,DEXM组心肌梗死面积(30.8±3.1)%,DEXM组梗死面积明显低于I/R组(P<0.05)。与Sham组及缺血前比较,I/R组和DEXM组缺血30 min及再灌注120 min时,HR、LVDP、±d P/dt均显著降低(P<0.05),LVEDP显著升高(P<0.05)。I/R组和DEXM组相比,DEXM相LVDP、±d P/dt均高于I/R组(P<0.05),LVEDP低于I/R组(P<0.05)。I/R组和DEXM组心肌组织中Ry R2和SERCA2a的m RNA水平均较Sham组降低(P<0.05),但DEXM组Ry R2和SERCA2a的m RNA水平高于I/R组。结论缺血再灌注前给予右美托咪定预处理可减小心肌梗死面积,促进心肌细胞钙循环,改善心功能,发挥心肌保护作用。Objective To investigate the protective effects of dexmedetomidine preconditioning in rats with myocardial ischemia reperfusion injury and the effects of dexmedetomidine on myocardium ryanodine receptor (RyR2) and sarcoplasmic reticIlum Ca2+-ATPase (SERCA2a). Methods Forty-five rats were randomly divided into three groups, sham operation group (Sham group), ischemia-reperfusion group (I/R group) and dexmedetomidine pre-conditioning group (DEXM group). 2 h before left anterior descending coronary artery clamped, DEXM group re-ceived dexmedetomidine 100μg/kg by intraperitoneal injection. The hemodynamic parameters were measured at the time of ischemia 30 min and reperfusion 120 min. The infarct size of myocardial tissues was determined by TTC stain-ing. The mRNA level of RyR2 and SERCA2a were detected by the Real-time PCR. Results The infarct size was (41.5±2.9)%in I/R group, which was significantly higher than (30.8±3.1)%in DEXM group (P〈0.05). Compared with the Sham group and the baseline before ischemic, heart rate (HR), left ventricular diastolic pressure (LVDP) and ±dP/dt decreased and the left ventricular end-diastolic pressure (LVEDP) increased in both I/R group and DEXM group at the time of ischemia 30 min and reperfusion 120 min (P〈0.05). Compared with the I/R group, LVDP and ±dP/dt were higher, and LVEDP was lower in the DEXM group. Compared with the Sham group, the mRNA level of RyR2 and SERCA2a were smaller in the I/R group and DEXM group, which were higher in DEXM group than in I/R group. Conclusion Dexmedetomidine preconditioning could attenuate myocardial ischemia reperfusion injury in rats via de-creasing infarct size, improving cardiac function and increasing the mRNA level of RyR2 and SERCA2a.

关 键 词:右美托咪定 预处理 缺血再灌注损伤 

分 类 号:R542.2[医药卫生—心血管疾病]

 

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