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.     

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。     

阿片类药物对乳腺癌血管生成及休眠的影响

【摘要】〓在乳腺癌综合治疗中,外科手术治疗占有重要地位,由此导致围术期镇痛药物的使用不可缺少。在围术期镇痛以及包括癌性疼痛在内的多种疼痛的治疗中,阿片类药物起着无可替代的作用,故部分乳腺癌患者在治疗过程中需使用阿片类药物。然而阿片类药物可能影响乳腺癌血管生成以及肿瘤细胞休眠、复发、转移,进而有可能影响乳腺癌患者的预后。因此,阿片类药物对于乳腺癌复发转移方面的影响不容忽视。     

葡聚糖接枝聚乳酸载吗啡缓释纳米粒胶束对急性疼痛大鼠的镇痛效应

目的:观察葡聚糖接枝聚乳酸载吗啡缓释纳米粒胶束(MP/DEX-PLA)对急性疼痛大鼠的镇痛效应.方法:SD雄性大鼠40只,随机均分为4组,A组(空白对照组),B组(空白纳米胶束对照组),C组(普通吗啡组),D组(载吗啡纳米胶束组).制备可生物降解的载吗啡葡聚糖接枝聚乳酸共聚物,皮下用药后测定急性疼痛大鼠的累计疼痛评分(CPS)和痛阈,评价药物的镇痛效果,观察其副作用.结果:MP/DEX-PLA纳米胶束呈球形,平均载药量为20.94%,平均包封率为36.27%.建模手术后,各组大鼠痛阈明显降低(P＜0.05);给药后,C组和D组CPS明显低于B组,痛阈明显升高(P＜0.05);C组和D组分别于给药后30 min和2h时达到最大镇痛效应,C组镇痛持续时间明显短于D组(P＜0.05),C组和D组痛阈最高值和CPS无明显差异(P＞0.05),C组不良反应发生率显著高于D组(P＜0.05).结论:皮下单次给予MP/DEX-PLA可通过吗啡缓慢释放发挥持续镇痛作用,副作用小于普通吗啡.     

术中异丙酚清醒镇静抗焦虑应激反应的作用

手术应激反应是病人对手术的恐慌、焦虑和紧张等心理反应与手术的生理干扰共同导致的民主自由综合征,与焦虑程度呈直线相关关系[1]。妇科手术病人的心理焦虑更为突出。蛛网膜下腔-硬膜外联合麻醉能够满足腹式全宫手术的镇痛、肌松需求。在我国,更由于手术费用的优势,椎管内麻醉占的比重还相当大。异丙酚清醒镇静是近年来我院麻醉科运用较广的术中抗焦虑方式,本研究对此抗焦虑作用作一个评价。1资料与方法1.1焦虑评分量表本实验采用的焦虑状态/特性询问表(state-traitanxiety inventory,STAI)是由Spielberger于1997编制,1983年修订的一种自…