右美托咪定预处理对大鼠心肌缺血-再灌注后心室功能和细胞凋亡的影响  

Effects of dexmedetomidine pretreatment on heart function and cell apoptosis after myocardial ischemia reperfusion injury in rats

作　　者：吴志林[1] 褚淑娟[1] 桂平[1] 伍静[1] 姚尚龙[1] 

机构地区：[1]华中科技大学同济医学院附属协和医院麻醉科,武汉市430022

出　　处：《临床麻醉学杂志》2015年第9期901-904,共4页Journal of Clinical Anesthesiology

摘　　要：目的探讨右美托咪定预处理对大鼠心肌缺血-再灌注损伤后心室功能和心肌细胞凋亡的影响。方法 30只SD大鼠随机分为三组,右美托咪定组(D组),右美托咪定+育亨宾组(D+Y组)和对照组(IR组),D组给予右美托咪定5μg·kg-1·h-1预处理1h,D+Y组静脉注射育亨宾1mg/kg,10min后按5μg·kg-1·h-1输注右美托咪定1h;IR组仅输注等量生理盐水,建立Langendorff缺血-再灌注模型,每10分钟测定左心室舒张末压(LVEDP)、左心室收缩压(LVSP)、左心室内压最大上升速率、下降速率(±dp/dtmax),计算左心室发展压(LVDP)。60min后取下心脏并以TUNEL检测心肌细胞的凋亡,RT-PCR检测Bcl-2mRNA,Bax mRNA的表达。结果与D组比较,再灌注后不同时点IR组和D+Y组大鼠LVDP、±dp/dtmax、Bcl-2mRNA表达明显降低、LVEDP、Bax mRNA表达明显升高(P<0.05)。IR组和D+Y组LVDP、LVEDP、±dp/dtmax、Bcl-2mRNA和Bax mRNA表达差异均无统计学意义。IR组细胞阳性率为(36.1±9.2)%、D+Y组为(38.2±6.5)%,明显高于D组为(24.0±8.3)%(P<0.05),而IR组和D+Y组细胞阳性率差异无统计学意义。结论右美托咪定预处理可以显著改善大鼠心肌缺血-再灌注损伤后的心室功能,并且可能通过调控凋亡基因Bcl-2mRNA和促凋亡基因BaxmRNA的表达,减少心肌细胞凋亡。Objective To investigate the effect on heart function and apoptosis of myocardial is- chemia reperfusion injury model with dexmedetomidine pretreatment in rats. Methods Thirty SD rats were randomly allocated to 3 groups： IR group, D group and D＋Y group. Dexmedetomidine was given to D group with an infusion rate of 5 μg· kg^-1 · h^-1 for 1 hour. Yohimbin （1 mg/kg）was given intravenously to D＋Y group 10 minutes before same dosage of dexmedetomidine as D group was giv- en. For IR group same amount of saline was infused. After the infusion, the heart was removed and Langendorff model of myocardial ischemia reperfusion injury was established quickly. Left ventricle function such as LVDP, LVEDP and ±dp/dtmax were recorded every 10 minutes. Cell apoptosis was detected with a TUNEL method. Bcl-2 mRNA and Bax mRNA were measured with real-time RT- PCR technique. Results Compared with group D, LVDP, ±dp/dtmax, the expression of Bcl-2 mR- NA were significantly lower, while LVEDP, the expression of Bax mRNA were significantly higher in group IR and group D＋Y at different time points after reperfusion（P〈0.05）. There was no signifi- cant difference in LVDP, LVEDP, ±dp/dtmax, the expression of Bcl-2 mRNA and Bax mRNA in group IR and group D＋Y. The positive rate of cell in group IR was （36.1±9.2）%, group D＋Y was （38. 2±6.5） %, significantly higher than group D （24±8. 3）% （P〈0.05）, there was no signif- icant difference between group IR and group D＋ Y. Conclusion Dexraedetomidine can dramatically improve left ventricle function and reduce cell apoptosis after ischemia reperfusion injury by modula- ting apoptotic related gene Bcl-2 mRNA and BaxmRNA expressions.

关 键 词：右美托咪定 心肌保护 缺血-再灌注损伤 细胞凋亡 

分 类 号：R614[医药卫生—麻醉学]