基础医学与临床 ›› 2017, Vol. 37 ›› Issue (8): 1103-1107.

• 研究论文 • 上一篇    下一篇

硬膜外罗哌卡因阻滞加强丙泊酚静脉麻醉的深度

崔旭1,赵晓艳1,张炳熙2,潘楚雄1,李俊发3   

  1. 1. 首都医科大学附属北京同仁医院
    2. 首都医科大学北京同仁医院
    3. 首都医科大学
  • 收稿日期:2016-07-29 修回日期:2016-09-29 出版日期:2017-08-05 发布日期:2017-07-17
  • 通讯作者: 李俊发 E-mail:junfali@ccmu.edu.cn
  • 基金资助:
    北京市优秀人才培养资助计划

Epidural ropivacaine block increasing anesthetic potency of propofol

  • Received:2016-07-29 Revised:2016-09-29 Online:2017-08-05 Published:2017-07-17
  • Contact: Jun-fa LI E-mail:junfali@ccmu.edu.cn

摘要: 目的 探讨硬膜外罗哌卡因阻滞对丙泊酚麻醉大鼠脑皮质和海马组织内Ca2+/钙调素依赖性蛋白激酶II(CaMKII)与细胞外信号调节蛋白激酶1/2(ERK1/2)蛋白表达及磷酸化水平的影响。方法 将大鼠随机分成丙泊酚组(对照组,P)、丙泊酚+硬膜外0.9%NaCl溶液组(PS)和丙泊酚+硬膜外罗哌卡因组(PR)3组,每组8只。硬膜外置管后72 h进行实验。PR组硬膜外给予0.5%罗哌卡因70 μL。所有大鼠经尾静脉输注1%丙泊酚,诱导剂量为12 mg/kg分次静脉注入,维持剂量为40 mg/kg/h。丙泊酚输注后1 h根据神经反射和对伤害性刺激的反应来评价麻醉深度。然后分离皮质和海马,用Western blot技术检测总蛋白(T-CaMKII、T-ERK1/ 2)和磷酸化(p-CaMKII、p-ERK1/ 2)水平。结果 P组有7只大鼠为浅麻醉,1只深麻醉;PS组有6只大鼠为浅麻醉,2只深麻醉;PR组有1只大鼠为浅麻醉,7只深麻醉,3组间麻醉深度不同(P<0.05)。 PR组海马组织中p-CaMKII(Thr286)和p-ERK1/2水平分别为(43.7±8.8)%和(32.4±7.9)%,显著低于P组(100%)(P<0.05)。结论 硬膜外0.5%罗哌卡因可加强丙泊酚静脉麻醉的深度,海马p-CaMKII、p-ERK1/2水平下降可能参与硬膜外阻滞作用。

关键词: 丙泊酚, 硬膜外阻滞, CaMKII, ERK1/2

Abstract: Objective The purpose of this study was to investigate the effects of epidural ropivacaine block combined with propofol intravenous anesthesia on CaMKII and ERK1/2 total protein (T-CaMKII and T-ERK1/2) and phosphorylation (p-CaMKII and p-ERK1/2) levels in the hippocampus and cortex of rats. Methods Rats were randomly assigned to three groups: group P(control, propofol intravenous anesthesia)、group PS( propofol and epidural normal saline) and group PR( propofol and epidural 0.5% ropivacaine). There were 8 rats in each group. Anesthesia were performed in 72 h after epidural catheter placement. The rats in group PR received 70 μL of 0.5% ropivacaine to achieve epidural block.1% propofol was infused through rats caudal vein. Propofol dosage for anesthesia induction was 12 mg/kg, for anesthesia maintenance was 40 mg/kg/h. Before the rats were decapitated,the depth of anaesthesia was assessed as either “light anesthesia” or “deep anesthesia” by checking of pinch withdrawal reflex, eyelid reflex and spontaneous rapid whisking of the vibrissae after propofol continuous infusion for 1 h. T-CaMKII/T-ERK1/2 and p-CaMKII/p-ERK1/2 in hippocampus and frontal cortex were examined by Western blot. Results 7 rats were assessed as “light anesthesia” and 1rat as “deep anesthesia” in group P; 6 rats were assessed as “light anesthesia” and 2 rats as “deep anesthesia” in group PS; In group PR, 1 rat was assessed as “light anesthesia” and 7 rats as “deep anesthesia”. Significant differences were seen among three groups (P<0.05). In hippocampus of rats, p-CaMKII(Thr286)(43.7±8.8)% and p-ERK1/2(32.4±7.9)% in group PR were significantly lower than those in group P (100%, P<0.05). Conclusions Epidural ropivacaine block could strengthen the depth of anesthesia achieved with propofol intravenous anesthesia. The decrease of the levels of p-CaMKII(Thr286) and p-ERK1/2 in hippocampus of rats may participate in the effects of epidural block.

Key words: Propofol, Epidural block, CaMKII, ERK1/2

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