持续输注利多卡因对腺样体切除术患儿麻醉苏醒期躁动的影响

目的　观察术中持续静脉泵注利多卡因对腺样体切除术患儿麻醉苏醒期躁动的影响。方法　选择2022年2月至6月在广东省妇幼保健院40例年龄在3～10岁,美国麻醉医师协会（ASA）分级Ⅰ～Ⅱ级择期在七氟烷全身麻醉下行腺样体切除术的患儿,按照随机数字表法将患儿分为生理盐水对照组（N组）及利多卡因持续静脉泵注组（L组）,每组各20例。N组男7例、女13例,年龄6（5,8）岁;L组男10例、女10例,年龄7（5,8）岁。患儿在诱导后,L组先静脉注射1 mg/kg利多卡因,继而以2 mg/（kg·h）持续静脉泵注利多卡因,N组给予等量生理盐水对照。主要结局指标包括躁动评分,躁动发生率,苏醒期麻醉药物追加次数;次要结局指标包括拔管后30 min疼痛评分,拔管时间及恢复室停留时间。采用独立样本t检验、Mann-Whitney U检验、Pearson Chi-Square检验。结果　L组患儿苏醒期WATCHA躁动评分较N组患儿低［1（0,2）分比3（0,4）分,P<0.05］,L组患儿躁动发生率低于N组［20%（4/20）比50%（10/20）,P<0.05］,L组患儿苏醒期麻醉药物追加率低于N组［15%（3/20）比60%（12/20）,P<0.01］。L组患儿拔管时间短于N组［（13.00±7.33）min比（19.40±7.39）min,P<0.01］,L组患儿恢复室停留时间短于N组［（42.00±7.85）min比（50.15±7.14）min,P<0.01］,L组患儿拔管后30 min疼痛评分低于N组［0（0,2）分比2（0,2）分,P<0.05］。结论　持续静脉泵注利多卡因可以减少腺样体切除术患儿麻醉苏醒期躁动的发生率,缩短拔管时间及恢复室停留时间,减轻术后疼痛,对加速患儿康复具有重要意义。     

右美托咪定用于吸毒患者悬雍垂腭咽成形术麻醉一例

患者,男,41岁,因"睡眠打鼾20余年,咽异物感5年"于2010年6月30日入院.患者既往有吸冰毒(甲基苯丙胺)史5年,每月3次,至今未戒.查体:神情倦怠,身高178cm,体重98 kg,体型肥胖,脖子粗短,下颌稍后缩,腭弓低垂,悬雍垂过长,咽腔狭小,Mallampati分级Ⅳ级.     

右美托咪定缓解神经病理性疼痛大鼠的痛觉过敏并抑制背根神经节内p-ERK信号通路的激活

目的 观察重复腹腔注射右美托咪定(DEX)对神经病理性疼痛大鼠的痛觉过敏和背根神经节(DRG)中ERK信号通路激活的影响.方法 给坐骨神经部分结扎(PSNL)神经病理性疼痛大鼠重复腹腔注射不同剂量的DEX.观察各组大鼠的机械、热痛觉过敏阈值.行为学测试完成后用免疫荧光和Western blot方法检测大鼠手术侧L5 DRG中p-ERK的表达.结果 (1)腹腔注射DEX 40 μg/kg 7、14 d均明显减轻PSNL诱导的机械、热痛觉过敏(P＜0.05).而腹腔注射DEX20μg/kg对PSNL大鼠疼痛行为学无明显影响.(2)重复腹腔注射40μg/kg DEX 7、14 d p-ERK的平均荧光强度比同一时间点的PSNL组明显减弱(P＜0.05),但仍明显高于对照组(P＜0.05).重复腹腔注射20μg/kg对PSNL大鼠p-ERK的平均荧光强度无明显影响(P＞0.05).(3)Westem blot 结果显示重复腹腔注射40μg/kg DEX 7、14 d明显抑制PSNL诱导的p-ERK的蛋白表达增多(P＜0.05).重复腹腔注射20μg/kg对PSNL大鼠p-ERK的蛋白表达无明显影响(P＞0.05).结论 重复腹腔注射DEX能够减轻神经损伤引起的痛觉过敏,抑制外周初级感觉神经系统中ERK信号通路的激活可能是其缓解的疼痛症状的机制之一.

Abstract：

Objective To investigate the effect of systemic administration of dexmedetomidine, a selective alpha 2 adrenergic receptor agonist, on mechanical and thermal hyperalgesia and dorsal root ganglia ERK activation induced by neuropathic pain. Methods Intraperitoneal injection of dexmedetomidine was repeatedly given once daily for 7 days or 14 days with the first injection one day before partial sciatic nerve ligation ( PSNL) surgery. Mechanical and thermal nociceptive thresholds were assessed in all animals. Then, animals were killed at corresponding time points, and the L5 DRG was removed for L5 DRG ERK activation status analysis by using immunoflurecence and Western blotting. Results (1) Partial sciatic never ligation produced a robust mechanical and thermal hyperalgisia and ERK activation of the L5 DRG in P7 and P14 groups. At the dose of 40 μg/kg, dexmedetomidine significantly attenuated PSNL-induced ipsilateral hyperalgesia on the day 7 and 14 after surgery. But the dose of 20 μg/kg of dexmedetomidine had no effect on pain behaviorl; (2) PSNL-induced up-regulation of mean fluorescence intensity of pERK on ipsilateral side of the L5 DRG was significantly suppressed by day 7, 14 post-PSNL following 40 μg/kg dexmedetomidine application, whereas 20 μg/kg dexmedetomidine had no effect; (3) Western blotting revealed that up-regulation of the protein expression of p-ERK on ipsilateral side of the L5 DRG was significantly inhibited on the day 7, 14 post-PSNL following 40 μg/kg dexmedetomidine application,whereas 20 μg/kg dexmedetomidine had no effect. Conclusion Systemic dexmedetomidine inhibits the activation of ERK signals in L5 DRG, which is possibly associated with its antihyperalgesia in rats with neuropathtic pain.     

右美托咪定缓解神经病理性疼痛大鼠的痛觉过敏并抑制背根神经节内p-ERK信号通路的激活

Objective To investigate the effect of systemic administration of dexmedetomidine, a selective alpha 2 adrenergic receptor agonist, on mechanical and thermal hyperalgesia and dorsal root ganglia ERK activation induced by neuropathic pain. Methods Intraperitoneal injection of dexmedetomidine was repeatedly given once daily for 7 days or 14 days with the first injection one day before partial sciatic nerve ligation ( PSNL) surgery. Mechanical and thermal nociceptive thresholds were assessed in all animals. Then, animals were killed at corresponding time points, and the L5 DRG was removed for L5 DRG ERK activation status analysis by using immunoflurecence and Western blotting. Results (1) Partial sciatic never ligation produced a robust mechanical and thermal hyperalgisia and ERK activation of the L5 DRG in P7 and P14 groups. At the dose of 40 μg/kg, dexmedetomidine significantly attenuated PSNL-induced ipsilateral hyperalgesia on the day 7 and 14 after surgery. But the dose of 20 μg/kg of dexmedetomidine had no effect on pain behaviorl; (2) PSNL-induced up-regulation of mean fluorescence intensity of pERK on ipsilateral side of the L5 DRG was significantly suppressed by day 7, 14 post-PSNL following 40 μg/kg dexmedetomidine application, whereas 20 μg/kg dexmedetomidine had no effect; (3) Western blotting revealed that up-regulation of the protein expression of p-ERK on ipsilateral side of the L5 DRG was significantly inhibited on the day 7, 14 post-PSNL following 40 μg/kg dexmedetomidine application,whereas 20 μg/kg dexmedetomidine had no effect. Conclusion Systemic dexmedetomidine inhibits the activation of ERK signals in L5 DRG, which is possibly associated with its antihyperalgesia in rats with neuropathtic pain.     

芬太尼复合右美托咪啶用于腰椎术后患者镇痛的效果

右美托咪啶(dexmeditomidine,DEX)是一种高效、高选择性α2肾上腺素能受体激动剂,具有剂量依赖性的镇静、镇痛、抗焦虑及交感神经抑制等作用[1],不良反应少。作者观察了芬太尼复合DEX用于腰椎术后患者的镇痛效果,报道如下。1对象与方法1.1研究对象60例ASAⅠ-Ⅱ级择期腰椎手术患者,年龄25~60岁,分为观察组和对照组,每组30例。术前用药为阿托品0.5mg和鲁米那0.1g肌内注射。1.2镇痛方法患者入室后静脉注射异丙酚2mg/kg、芬太尼2μg/kg、琥珀胆碱1.5mg/kg行麻醉诱导插管。术中以七氟醚和阿曲库铵维持麻醉。2组术毕均连接静脉自控镇痛泵。观察组给予芬太尼20μg/kg+止吐药帕洛诺司琼0.25mg+DEX2μg/kg,生理盐水稀释至100mL,对照组给予芬太尼20μg/kg+帕洛诺司琼0.25mg,生理盐水稀释至100mL。     

Toll样受体4单克隆抗体预处理对脂多糖诱发小鼠急性肺损伤的影响

目的 探讨预先使用Toll样受体4单克隆抗体(TLR4mAb)对LPS诱发的小鼠脓毒症肺损伤的保护作用.方法 45只健康清洁级雄性BALB/c小鼠以随机数字法分为对照组(C 组)、脓毒症组(S组)、预处理组(P组),每组15只.P组小鼠在造模前1h预先腹腔注射TLR4mAb 5 μg/g.S组、P组均腹腔注射LPS 10 mg/kg以制备脓毒症急性肺损伤模型,C组经腹腔注射等量生理盐水.各组分别于注射后6,12,24h,采用酶联免疫吸附法测定血清TNF-a和IL-6浓度;取肺脏组织,分别检测TLR4 mRNA的表达、肺组织含水量、病理学改变.组内比较采用双因素方差分析,组间比较采用单因素方差分析,以P ＜0.05为差异有统计学意义.结果 与C组比较,S组、P组肺组织含水量在12,24h时均显著性升高;与S组比较,P组肺组织含水量在12,24h时均显著性降低.与C组比较,S组、P组血清IL-6,TNF-α质量浓度在各时点均显著性升高;与S组比较,P组IL-6,TNF-α质量浓度在各时点均显著性降低.与C组比较,S组、P组TLR4 mRNA在各时点时均显著性升高;与S组比较,P组TLR4mRNA在各时点均显著性降低.与S组比较,P组病理改变程度均明显减弱.结论 预先使用TLR4mAb可以减轻LPS所诱发的急性肺损伤程度,可抑制炎性因子的过度表达;调控TLR4通路可能是治疗脓毒症及其肺损伤的有效靶点.     

Truview EVO2喉镜用于模拟颈椎固定致困难气道的研究

目的:评估麻醉住院医师在人体模型模拟颈椎固定致困难气道上使用Truview EVO2喉镜的效果.方法:20位未有在人体使用Truview EVO2喉镜经验的麻醉科住院医师,在高级麻醉医生讲解该喉镜使用方法并指导其在人体模型上以正常插管体位下成功完成3次插管,然后分别使用Macintosh喉镜和Truview EVO2喉镜在模型模拟颈椎后仰不能的情况下进行插管,记录喉镜暴露时间、插管时间、失败次数、喉镜暴露分级(C-L分级),并由受试者评定插管困难程度和对两种喉镜的喜好.结果:与Macintosh喉镜相比,Truview EVO2喉镜能显著改善颈椎后仰不能情况下的C-L分级(P＜0.05),但并不缩短插管所耗时间和减少失败次数.受试者评价Truview EVO2插管困难程度与Macintosh喉镜无显著差异.结论:与传统插管方法相比,Truview EVO2用于人体模型模拟颈椎固定所致困难气道时可显著改善声门暴露,但对于使用经验不足的操作者并不能缩短插管时间.     

NI指数与右美托咪定镇静深度相关性研究

目的:观察Narcotrend指数NI与右美托咪定镇静深度的相关性.方法:选择择期在腰硬联合麻下行膝关节镜手术的患者20例,年龄18-40岁,体重50-90 kg,腰硬联合穿刺20 min后,依次微泵输注右美托咪定,0.05 μg/( kg·min),0.1 μg/(kg·min),0.2 μg/(kg·min)各3 min,停药后唤醒.记录输注右美托嘧啶前(T0)、输注0.05 μg/(kg·min)3 min后(T1)、输注0.1 μg/(kg·min)3 min后(T2)、输注0.2 μg/(kg·min)3 min后(T3)、唤醒后1 min(T4)的NI指数.结果:随着右美托咪定泵注速度的增加,脑电意识深度NI指数都有不同程度的降低,唤醒后NI指数回升.Spearman相关系数为r＝-0.7643,P＜0.05.结论:Narcotrend的NI指数能很好的评价右美托咪定的镇静水平.     

慢性吗啡处理对C6细胞EAAT3蛋白表达的影响及其机制研究

目的探讨慢性吗啡暴露、戒断、再次暴露对C6细胞兴奋性氨基酸转运蛋白3(excitatory amino-acid transporter 3,EAAT3)蛋白表达的影响及可能机制。方法 0.1～10μmol·L-1吗啡作用于C6细胞不同时间,Western blot检测C6细胞EAAT3蛋白表达水平变化,然后用不含吗啡的培养液培养细胞模拟吗啡自然戒断过程,待EAAT3蛋白表达回升后,再次吗啡暴露(吗啡浓度为第1次给药的1/2)模拟吗啡复吸过程,观察吗啡多次暴露对C6细胞EAAT3蛋白表达的影响。最后在吗啡再次暴露前15 min使用纳洛酮,观察纳洛酮对多次吗啡暴露引起的C6细胞EAAT3表达变化的影响。结果 10μmol·L-1吗啡作用于C6细胞至少48 h可下调C6细胞EAAT3蛋白表达(P<0.05)。停用吗啡至少12 h后,EAAT3蛋白表达回升,5μmol·L-1吗啡再次处理C6细胞4 h即可下调C6细胞EAAT3蛋白表达水平(P<0.05)。1μmol·L-1纳洛酮可明显抑制慢性吗啡处理引起的EAAT3蛋白表达下降(P<0.05)。结论慢性吗啡处理可下调C6细胞EAAT3表达水平,停用吗啡EAAT3表达回升,吗啡再次暴露引起EAAT3表达水平下降所需吗啡浓度降低,暴露时间缩短。吗啡通过作用于阿片受体诱导C6细胞EAAT3表达下降。