地塞米松对布比卡因诱导小鼠神经元毒性的影响

Objective To investigate the effect of dexamethasone on the toxicity of bupivacaine in murine neurons.Methods Murine neuroblastoma cell line N2a was obtained from ATCC cell bank (USA). The cells were cultured in 10% fetal cow serum/MEM culture medium and divided into 4 groups voup I control (Con); group II bupivacaine ( Bup); group Ⅲ dexamethasone (Dex) and group IV Dex + Bup. The culture medium contained bupivacaine 900 μmol/L in group Bup and dexamethasone 1 μmol/L in group Dex respectively. In group Dex + Bup ( IV ) Bup was added to the culture medium with a final concentration of 900 μmol/L at 12 h after pretreatment with Dex 1 μmol/L. The cells were inoculated in 24 well plates (0.5 ml in each well, 24 wells in each group) and 10 cm culture dishes (7 ml in each dish, 4 dishes in each group). The release rate of LDH was calculated and the morphology of the cells and nucleus condensation (by Hoechst 3334224 fluorescent staining) was detected at 9 h of incubation in 24 well plates. The mitochondrial transmembrane potential (by JC-1 assay) and phosphorylation of Akt and ERKs (by Western blot) were measured at 5 h of incubation in 24 well plates and in culture dishes respectively. ResultsBupivacaine caused severe damage to the N2a cells as evidenced by increase in LDH release and nucleus condensation (apoptosis), dephosphorylation of Akt and ERKs, decrease in mitochondrial transmembrane potential and severe morphological changes. Dexamethasone pretreatment significantly attenuated bupivacaine-induced neurotoxicity. Conclusion Dexamethasone can protect N2a cells from bupivacaine-induced neurotoxicity through stabilization of mitochondrial transmembrane potential and inhibition of dephosphorylation of Akt and ERKs.     

地塞米松对布比卡因诱导小鼠神经元毒性的影响

Objective To investigate the effect of dexamethasone on the toxicity of bupivacaine in murine neurons.Methods Murine neuroblastoma cell line N2a was obtained from ATCC cell bank (USA). The cells were cultured in 10% fetal cow serum/MEM culture medium and divided into 4 groups voup I control (Con); group II bupivacaine ( Bup); group Ⅲ dexamethasone (Dex) and group IV Dex + Bup. The culture medium contained bupivacaine 900 μmol/L in group Bup and dexamethasone 1 μmol/L in group Dex respectively. In group Dex + Bup ( IV ) Bup was added to the culture medium with a final concentration of 900 μmol/L at 12 h after pretreatment with Dex 1 μmol/L. The cells were inoculated in 24 well plates (0.5 ml in each well, 24 wells in each group) and 10 cm culture dishes (7 ml in each dish, 4 dishes in each group). The release rate of LDH was calculated and the morphology of the cells and nucleus condensation (by Hoechst 3334224 fluorescent staining) was detected at 9 h of incubation in 24 well plates. The mitochondrial transmembrane potential (by JC-1 assay) and phosphorylation of Akt and ERKs (by Western blot) were measured at 5 h of incubation in 24 well plates and in culture dishes respectively. ResultsBupivacaine caused severe damage to the N2a cells as evidenced by increase in LDH release and nucleus condensation (apoptosis), dephosphorylation of Akt and ERKs, decrease in mitochondrial transmembrane potential and severe morphological changes. Dexamethasone pretreatment significantly attenuated bupivacaine-induced neurotoxicity. Conclusion Dexamethasone can protect N2a cells from bupivacaine-induced neurotoxicity through stabilization of mitochondrial transmembrane potential and inhibition of dephosphorylation of Akt and ERKs.     

右美托咪定对尿毒症行甲状旁腺切除术患者围术期超敏肌钙蛋白T的影响

目的：探讨右美托咪定对尿毒症行甲状旁腺切除术患者围术期超敏肌钙蛋白T（hypersensitivity troponin T,hs?cTNT）的影响。方法：选择因尿毒症肾功能衰竭继发甲状旁腺功能亢进择期行甲状旁腺切除术的患者60例,年龄18~60岁,美国麻醉医师协会（ASA）分级Ⅱ~Ⅲ级,预计手术时间在2 h内。将患者随机分为对照组（C组）和右美托咪定组（D组）。D组患者麻醉诱导前静脉泵注右美托咪定1 μg/kg,后以0.2 μg/（kg·h）的速度泵注至手术结束前30 min;C组患者静脉输注同等量的生理盐水。记录两组患者术前（T0）、手术开始时（T1）、手术结束时（T2）、手术结束30 min（T3）、术后（T4）的心率（heart rate,HR）和平均动脉压（mean arterial pressure,MAP）;记录两组患者术前和术后1 d的hs?cTNT值;记录两组患者术后不良反应（恶心和呕吐）的发生率。结果：两组患者在各时间点的HR和MAP相比差异无统计学意义（P > 0.05）;两组患者间术前hs?cTNT比较,差异无统计学意义（P > 0.05）,但在术后1 d时D组hs?cTNT明显低于C组（P＜0.05）;两组术后不良反应的发生率无明显差异（P > 0.05）。结论：右美托咪定用于尿毒症行甲状旁腺切除术的患者可降低术后hs?cTNT水平,对心肌有一定的保护作用。     

HSPA12A高表达于神经组织

目的研究热休克蛋白70(HSP70)家族新成员HSPA12A的组织分布和细胞定位。方法采用免疫印迹和免疫荧光组织化学方法,分析成年小鼠7种不同组织中HSPA12A的表达,并探讨其是否在成年、胚胎鼠神经元中具有表达。结果 (1)在成年小鼠心、肝、脾、肺、肾、脑、骨骼肌这7种组织中,脑组织的表达量是其他组织的至少10倍以上(P<0.01);(2)HSPA12A在胚胎时期的鼠皮层神经元中表达;(3)HSPA12A在成年鼠的皮层神经元中持续表达。结论 HSPA12A被首次证实在神经组织中表达最高,且从胚胎时期到成年鼠皮层神经元中均持续表达,提示HSPA12A可能在神经细胞的内稳态维持中具有重要作用。     

心脏手术停机困难的回顾性分析

我国风湿性心脏病发病率较高,其瓣膜病变常需要外科手术治疗,这种瓣膜手术需要借助体外循环的辅助使心脏停止跳动才能得以进行,某些患者往往在经过手术修复或置换心脏瓣膜后,因为种种原因不能即刻脱离体外循环。为此,我们回顾性分析了我院2008年1月-2010年12月,1500例行体外循环的风湿性心脏病患者中41例停机困难的原因。     

酚妥拉明在嗜铬细胞瘤手术中的应用

目的评价嗜铬细胞瘤手术中防御性给予酚妥拉明对维持血流动力学稳定的效果.方法选择术前诊断并经术后病理检查证实为嗜铬细胞瘤的患者30例,美国麻醉医师学会分级Ⅱ或Ⅲ级根据使用降压药种类和方式的不同分为3组,每组10例硝普钠组经微量静脉输液泵注射0.01%硝普钠酚妥拉明1组经微量静脉输液泵注射0.08%酚妥拉明酚妥拉明2组分别于麻醉诱导时和切皮前2min静脉注射酚妥拉明5mg,分离瘤体前2min静脉注射酚妥拉明10mg术中根据血压和心率(HR)的变化给予乌拉地尔或艾司洛尔记录麻醉前(T0)、探查肿瘤前(T1)、探查肿瘤时(T2)、肿瘤血管阻断时(T3)和术毕(T4)5个时间点的收缩压(SBP)、HR、中心静脉压(CVP)以及血管活性药物使用情况结果 3组间在T0时间点的SBP的差异均无统计学意义(P值均>0.05);在T1时间点有升高趋势,但差异无统计学意义(P值均>0.05);3组在T2时间点的SBP均显著高于同组T0时间点(P值均<0.05),硝普钠组、酚妥拉明1组均显著高于酚妥拉明2组(P值均<0.05);3组在T3、T4时间点的SBP均有低于同组T0时间点的趋势,但差异均无统计学意义(P值均>0.05),3组间差异也均无统计学意义(P值均>0.05)3组间在同时间点的HR和CVP的差异均无统计学意义(P值均>0.05)硝普钠组、酚妥拉明1组的乌拉地尔用量显著多于酚妥拉明2组(P值均<0.01),酚妥拉明1组的酚妥拉明用量显著多于酚妥拉明2组(P<0.01),3组间艾司洛尔和去甲肾上腺素用量的差异均无统计学意义(P值均>0.05)结论在术前准备充分的情况下,在进行嗜铬细胞瘤麻醉手术中易引起血流动力学波动的主要操作步骤时防御性给予酚妥拉明,可有效维持患者的循环稳定,并可减少其他降压药的用量     

急性呼吸窘迫综合征的肺泡表面活性物质补充治疗

对近几年急性呼吸窘迫综合征肺泡表面活性物质补充治疗,特别是肺灌洗补充治疗的机制、疗效作一综述。     

肺泡表面活性物质灌洗的浓度和时间对急性呼吸窘迫综合征治疗效果的影响

目的 观察肺泡表面活性物质(SF)灌洗的浓度和时间对急性呼吸窘迫综合征(ARDS)治疗效果的影响.方法 用0.0225N盐酸12 ml/kg注入新西兰白兔气管内,建立ARDS模型后随机分成七组,每组5只.在盐酸注入后1h用浓度为1、3、6和12g/L的SF肺灌洗,2和3h用浓度为12 g/L的SF肺灌洗;对照组用生理盐水灌洗.观察治疗前后二氧化碳分压(PaCO2)和气道吸气峰压(PIP)变化;并对肺标本行病理检查.结果 造模1h后,3、6和12 g/L的SF灌洗均明显降低PaCO2,作用持续1.5h;造模2h后用浓度为12 g/L灌洗组PaCO2降低作用可持续2h.但3h组PaCO2未见降低.各灌洗组均不能降低PIP.结论 盐酸造模后2h内进行SF 3～12 g/L肺灌洗可改善肺换气功能.     

低体重婴儿先天性心脏病矫治术的麻醉管理

目的 总结16例体重≤5kg的婴儿先天性心脏病矫治术的麻醉管理.方法 常规麻醉诱导,气管插管,动静脉置管测压,体外循环下完成手术,合理使用血管活性药物维持血流动力学.结果全组有1例行体肺动脉分流术的患儿死亡,其余恢复良好.结论 低体重婴儿先天性心脏病矫治术的围术期麻醉管理较困难,并发症多,正确处理可降低其并发症及术后带机时间.     

异氟醚对心肌细胞超微结构及CX43蛋白表达的保护作用

目的 观察异氟醚预处理对缺血/再灌注心肌细胞超微结构及CX43蛋白表达的保护作用.方法 连续观察54例心脏瓣膜疾病接受瓣膜置换的病人,随机分为观察组(异氟醚处理)和对照组(非异氟醚处理).体外循环前后剪取右心耳组织标本处理,电子显微镜下观察心肌细胞超微结构的变化,免疫组化方法测定心肌纤维CX43蛋白表达水平,并作图像定量分析.对比手术前后超声心动图心功能指标.结果 观察组心肌细胞线粒体和闰盘结构基本完整,CX43表达水平稳定.对照组心肌细胞超微结构破坏严重,CX43表达水平明显降低(P<0.05).结论 异氟醚能维持体外循环后心肌细胞CX43蛋白表达的稳定,保护了心肌细胞超微结构的完整性,有利于术后心功能恢复.