薛凯凯, 杨玲, 陈海明. 右美托咪定联合远隔缺血预处理对心肌缺血/再灌注损伤的影响[J]. 心脏杂志, 2019, 31(3): 302-305. DOI: 10.12125/j.chj.201811016
    引用本文: 薛凯凯, 杨玲, 陈海明. 右美托咪定联合远隔缺血预处理对心肌缺血/再灌注损伤的影响[J]. 心脏杂志, 2019, 31(3): 302-305. DOI: 10.12125/j.chj.201811016
    Kai-kai XUE, Ling YANG, Hai-ming CHEN. Effects of dexmedetomidine combined with limb remote ischemic preconditioning on myocardial ischemia-reperfusion injury[J]. Chinese Heart Journal, 2019, 31(3): 302-305. DOI: 10.12125/j.chj.201811016
    Citation: Kai-kai XUE, Ling YANG, Hai-ming CHEN. Effects of dexmedetomidine combined with limb remote ischemic preconditioning on myocardial ischemia-reperfusion injury[J]. Chinese Heart Journal, 2019, 31(3): 302-305. DOI: 10.12125/j.chj.201811016

    右美托咪定联合远隔缺血预处理对心肌缺血/再灌注损伤的影响

    Effects of dexmedetomidine combined with limb remote ischemic preconditioning on myocardial ischemia-reperfusion injury

    • 摘要:
        目的  研究右美托咪定联合远隔缺血预处理对心肌缺血/再灌注损伤(MI/RI)的影响以及探讨其对细胞凋亡的影响
        方法  选取80例择期体外循环下行心脏瓣膜术病患,随机分成4组(n = 20);对照组(C组), 远隔缺血预处理组(R组),右美托咪定组(D组),右美托咪定联合远隔缺血预处理组(DR组);R组于麻醉诱导后行上肢缺血预处理,D组将盐酸右美托咪定以1 μg/kg负荷剂量泵注10 min后以0.41 μg/ (kg·h)注入至手术结束,DR组联合应用D组和R组两种方法;测主动脉阻断前(T0)、体外循环结束时(T1)和结束手术后(T2)血浆肌钙蛋白I(cTnI)浓度。检测T0和T1 时Bcl-2和Bax蛋白含量及计数心肌细胞凋亡指数(AI)。
        结果  T1和T2时,与对照组比较,各组血浆cTnI均降低(P<0.05)。与阻断主动脉前相比,体外循环结束后4组心肌组织Bcl-2、Bax蛋白值含量和AI均升高,Bcl-2/Bax下降(P<0.05);与C组比较,D组、R组和DR组Bcl-2、Bcl-2/Bax均增高,Bax和AI降低(P<0.05);与R组、D组比较,DR组Bcl-2、Bcl-2/Bax升高,Bax和AI降低(P<0.05)。
        结论  右美托咪定与远隔缺血预处理均能减轻MI/RI,二者联合作用优于单独使用,其机制可能与抑制细胞凋亡有关。

       

      Abstract:
        AIM  To study the effects of dexmedetomidine combined with remote ischemic preconditioning on myocardial ischemia reperfusion injury and to evaluate its effect on apoptosis.
        METHODS  Eighty patients scheduled for heart valve replacement under cardiopulmonary bypass were randomly divided into 4 groups (n = 20): a control group (group C), a limb ischemia preconditioning group (group R), a dexmedetomidine pretreatment group (group D), and a dexmedetomidine pretreatment combined with limb ischemia preconditioning group (group DR). Group R received upper limb ischemic preconditioning after induction of anesthesia. In group D, dexmedetomidine was intravenously administered as a loading dose of 11 μg/kg for 10 min and then intravenously 0.41 μg/(kg·h) until the completion of the operation. Plasma troponin I (cTnI) levels were measured before aortic occlusion (T0), at the end of cardiopulmonary bypass (T1) and after the operation (T2). The contents of Bcl-2 and Bax protein and cardiomyocyte apoptosis index (AI) were measured before aortic occlusion and at the end of cardiopulmonary bypass.
        RESULTS  Compared with group C, at T1 and T2, plasma cTnI decreased in all the other groups (P < 0. 05). Compared with those before aortic clamping, Bcl-2, Bax protein content and AI in the cardiac tissues of the four groups increased, and Bcl-2/Bax decreased after CPB (P < 0.05). Compared with those in group C, the protein of Bcl-2 and Bcl-2/Bax increased and the protein of Bax and AI decreased in group D, group R and group DR (P < 0.05). Compared with those in group R and D, the content of Bcl-2 and Bcl-2/Bax protein in the DR group increased and the value of Bax protein and AI decreased (P < 0.05).
        CONCLUSION  Dexmedetomidine and limb remote ischemic preconditioning reduce myocardial ischemia reperfusion injury and the combined effects of the two are superior when compared to individual results. Inhibition of cell apoptosis is likely mechanisticly involved.

       

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