骶管腔注入氯胺酮复合罗哌卡因在小儿脐以下手术中的应用

目的：探讨骶管腔内注入氯胺酮复合罗哌卡因对于小儿脐以下手术围麻醉期的麻醉效果。方法：69例ASAⅠ或Ⅱ级择期行脐以下手术的患儿随机分为三组行骶管阻滞。第一组（R组，n=23）骶管腔给予罗哌卡因0.2%1mL/kg；第二组（K组，n=23）给予氯胺酮0.5mg/kg；第三组（RK组，n=23）给予罗哌卡因0.2%1mL/kg加氯胺酮0.25mg/kg。使用视觉类比量表行疼痛评分，若疼痛评分大于3即静脉给与镇痛药芬太尼0.5～1μg/kg。记录骶管阻滞所引起的相关副作用及额外镇痛药芬太尼的需要量。结果：RK组病人的麻醉无痛时间长于R组和K组（P〈0.05），三组并发症的发生率无统计学差异。结论：氯胺酮复合罗哌卡因可安全用于小儿骶管阻滞，延长麻醉镇痛时间。     

先天性食管闭锁手术的麻醉处理

目的：探讨先天性食道闭锁修补术的合理麻醉处理。方法：回顾性分析我院自1999年以来18例先天性食道闭锁修补术的麻醉处理经过。结果：本组18例患儿均采用气管插管全麻，全部病例术中无1例死亡。术后3例分别因心功能衰竭和严重肺炎死亡，余15例均存活出院。术中有4例患儿出现明显胃胀。通气困难．通过将导管继续送人气管少许或由术者暂时阻断瘘管均可改善通气。本组病例整个手术过程补液速度平均11．6mL/(kg．h)。结论：先天性食道闭锁修补术的合理麻醉处理应包括充分的术前准备、严格的呼吸循环管理及严密的监测。     

顺式阿曲库铵不同用药方式对老年全凭静脉麻醉肌松作用的影响

目的 探讨顺式阿曲库铵不同用药方式对老年患者全凭静脉麻醉肌松作用的影响.方法 60例掸期在全麻下行普外科手术的老年患者,ASA I～Ⅱ级.年龄7l～87岁,随机分为A组(η=20)和B组(η=40),其中B组再随机分为B1组(η=20)和B2组(η=20).肌松诱导:A组单次予顺式阿曲库铵0.2 mg·kg-1静注;B...     

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。     

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.     

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。     

怕痛，还是怕成瘾

说起止痛药,大家对它的印象似乎总会伴随几个不是特别褒义的词：治标不治本、成瘾。对于止痛药成瘾的问题,甚至一部分人认为,这止痛药就和毒品差不多,吃久了会上瘾．停不了。这使得不少人对止痛药嗤之以鼻,到了医生给自己开了止痛药的时候往往会陷入矛盾之中,一方面自己有不得不使用止痛药的疼痛,另一方面又害怕成瘾,到底是要怕疼还是要怕成瘾呢？     

姜黄素预处理对大鼠脑缺血/再灌注损伤后AQP-4及脑水肿的影响

目的研究化学合成的姜黄素预处理对大鼠脑缺血/再灌注损伤后AQP-4及脑水肿的影响。方法采用线栓法阻塞大鼠大脑中动脉(MCAO),建立大鼠局灶性脑缺血/再灌注实验模型,72只SD大鼠被随机分为假手术组(S组)、缺血/再灌注组(I组)和姜黄素(缺血前30 min腹腔给予50、100 mg.kg-1)组(C1和C2组),每组18只。I组和C1、C2组分别在脑缺血/再灌注后24 h处死。观察大鼠神经功能缺失的评分;干湿重法观察大鼠脑含水量的变化,通过收集透出脑血管外的伊文思蓝(EB)来示踪血脑屏障(BBB)的变化,免疫印记法检测AQP-4和c-Jun氨基端激酶(JNK)的表达情况。结果 S组无神经行为改变;C1、C2组脑含水量、EB量、AQP-4表达及JNK磷酸化水平与I组相比明显降低(P<0.05);C1、C2组神经学评分高于Ⅰ组(P<0.05)。结论化学合成的姜黄素可减轻大鼠局灶性脑缺血/再灌注后AQP-4表达水平及BBB的破坏程度,减轻脑水肿,其机制可能与抑制JNK通路的磷酸化激活有关。