标题：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

      作者：李 霞 1，2，彭碧文 1，董 航 2
    (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)

      卷次： 2015年26卷18期

      【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(RyR2)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100 μg/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RyR2和SERCA2a的mRNA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、±dP/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、±dP/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RyR2和 SERCA2a的mRNA水平均较 Sham组降低(P<0.05)，但
DEXM组RyR2和SERCA2a的mRNA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。

      【关键词】 右美托咪定；预处理；缺血再灌注损伤

      【中图分类号】 R542.2 【文献标识码】 A 【文章编号】 1003—6350（2015）18—2668—03


Protective effects of dexmedetomidine preconditioning in rats with myocardial ischemia reperfusion injury and
the effects on calcium regulatory proteins.
LI Xia 1,2, PENG Bi-wen 1, DONG Hang 2. 1. School of Basic Medical
Sciences, Wuhan University, Wuhan 430000, Hubei, CHINA; 2. Department of Anesthesiology, the Affiliated Hospital of
Jianghan University, Wuhan 430000, Hubei, CHINA

【Abstract】 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 100 μg/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.

      【Key words】 Dexmedetomidine; Preconditioning; Ischemia reperfusion injury