Delta阿片受体参与低氧预处理减轻心肺复苏脑损伤的研究  

Involvement of delta opioid receptor in the neuroprotection induced by hypoxic preconditioning in the asphyxial cardiac arrest rat model

作　　者：高昌俊[1] 孙绪德[1] 张贵和[1] 牛江涛[1] 蒯建科[1] 柴伟[1] 

机构地区：[1]第四军医大学唐都医院麻醉科,陕西省西安市710038

出　　处：《临床麻醉学杂志》2012年第5期488-490,共3页Journal of Clinical Anesthesiology

基　　金：国家自然科学基金面上项目(81071527)

摘　　要：目的研究delta阿片受体(DOR)是否参与了低氧预处理(HPC)对心肺复苏大鼠脑损伤的保护作用。方法 90只大鼠接受为期7d的HPC后,建立大鼠窒息性心肺复苏脑损伤模型,随机均分为五组:心跳停止(CA)组(A组)、HPC+CA组(B组)、Naltrindole(NTI,DOR特异性拮抗药)+CA组(C组)、HPC+人工脑脊液(ACSF)+CA组(D组)及HPC+NTI+CA组(E组)。A组仅建立心肺复苏模型;C组大鼠在窒息前30min经侧脑室注入含50nmolNTI的ACSF10μl;B、D、E组均接受连续7d的HPC,HPC结束后24h,B组大鼠接受气管插管、8min窒息以及心肺复苏;而D组和E组大鼠则在窒息前30min分别经侧脑室注入含0或50nmolNTI的ACSF10μl。观察复苏成功率并对存活大鼠的神经功能缺损进行评分,观察复苏后海马CA1区神经元损伤及凋亡情况。结果 HPC改善心肺复苏脑损伤后的神经功能缺损,抑制早期海马神经元的凋亡,增加海马CA1区存活神经元的数量,而DOR拮抗药Naltrindole明显消除了HPC的神经保护作用。结论在HPC减轻心肺复苏大鼠脑损伤的过程中,DOR发挥着重要作用。Objective To investigate whether DOR is involved in the neuroprotection induced by hypoxic preconditioning （HPC） in cardiac arrest （CA） rat. Methods Twenty-four hours after the end of 7-day HPC, CA was induced by 8-rain asphyxiation in rats and the animals were resuscitated with a standardized method. The survival rate after resuscitation was recorded. The neurological deficit score （NDS）, neuronal apoptosis and the number of viable hippocampal CA1 neurons were evaluated at 24 h, 72 h or 7 days after restoration of spontaneous circulation in the presence or absence of naltrindole （a selective DOR antagonist）. Results HPC improved neurological outcome, inhibited neuronal apoptosis, and increased the number of viable hippocampal CA1 neurons after ROSC. The beneficial effects were abolished by the DOR antagonist naltrindolc. Conclusion DOR plays important roles in the neuroprotection induced by HPC in CA rat model.

关 键 词：心跳停止 全脑缺血 大鼠 Delta阿片受体 低氧预处理 

分 类 号：R614[医药卫生—麻醉学]