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.     

血管活性药物对盐酸吸入性肺损伤大鼠动脉血氧分压的影响

目的 研究血管活性药物对急性肺损伤(ALI)大鼠动脉血氧分压(PaO2)的影响.方法 28只SD大鼠随机均分为四组,分别静注生理盐水(A组)、艾司洛尔加硝酸甘油(B组),艾司洛尔加去氧肾上腺素(C组)和异丙肾上腺素(D组).然后均经气管导管内注入0.1 N盐酸1mlkg造成ALI.记录静脉注入实验药物即刻(T0)、气管注入盐酸后10 min(T1)和30 min(T2)的PaO2、MAP、HR值.结果 各组T1和T2时的PaO2均较T0时明显下降(P<0.01).C组T1和T2时的PaO2明显低于其他组(P<0.01),而D组PaO2的下降幅度最小,显著高于其他各组(P<0.01).结论 异丙肾上腺素能减轻ALI,合用艾司洛尔和去氧肾上腺素则恶化ALI.     

羟考酮抑制前列腺电切术患者气管插管反应及膀胱刺激征的效果观察

目的: 观察并比较前列腺电切术患者给予单次剂量羟考酮或芬太尼的气管插管反应及术后导管相关膀胱刺激（CRBD）的治疗效果。方法: 选取全身麻醉下行气管插管前列腺电切术患者60例,根据随机数字表法分别纳入羟考酮组和芬太尼组,每组30例,在麻醉诱导前2 min分别给予羟考酮(0.2 mg/kg)或芬太尼(2 μg/kg),观察气管插管前后心率、血压的变化,两组患者用药后眩晕、嗜睡等发生率,拔管后0、0.5、2、6 h内CRBD的发生率和严重程度,术后静脉镇痛药的需求情况。结果： 两组患者麻醉诱导前后心率和平均动脉压的变化值无显著差异(P>0.05),给药后两组眩晕嗜睡等发生率无明显差异(P>0.05);与芬太尼组相比,羟考酮组拔管后0、0.5、2 hCRBD发生率低(P<0.05);所需静脉镇痛药物更少(P<0.05)。结论： 单次剂量的羟考酮可安全有效地用于前列腺电切手术患者,抑制其气管插管反应;与芬太尼相比,羟考酮可降低术后早期CRBD的发生。     

失能老年人长期照护质量评价指标体系的构建

目的 构建失能老年人长期照护质量评价指标体系,旨在推进和完善我国失能老年人的长期照护服务。方法 在文献研究、小组讨论和预调查的基础上拟定指标体系初稿,通过德尔菲法对北京市25名专家进行2轮函询。结果 2轮专家函询问卷的有效回收率分别为93%和100%,专家权威系数为0.926。第2轮专家函询时,一、二、三级指标的专家意见协调系数分别为0.427、0.501和0.552（P＜0.001）,变异系数均＜0.25。最终确立的失能老年人长期照护质量评价指标体系,包括3项一级指标、14项二级指标和80项三级指标。结论 失能老年人长期照护质量评价指标的可靠性较好,内容全面、科学,明确了照护服务的内容,为提高失能老年人照护服务质量提供借鉴。     

右美托咪定复合布托啡诺在剖宫产术后镇痛的应用

目的研究右美托咪定复合布托啡诺用于剖宫产术产妇自控静脉镇痛(PCIA)的安全性和临床效果。方法选择择期硬膜外麻醉下行剖宫产术产妇60例,年龄24～43岁,身高153～171cm,体重53～93kg,ASAⅠ或Ⅱ级,采用随机数字表法将产妇分为两组(n=30)。对照组(C组):胎儿娩出断脐后静脉给予生理盐水30ml,术后PCIA(布托啡诺3μg·kg~(-1)·h~(-1),背景输注速率2ml/h,每次按压0.5ml,锁定时间10min);右美托咪定组(D组):胎儿娩出断脐后静脉给予右美托咪定0.5μg/kg,术后PCIA(布托啡诺3μg·kg~(-1)·h~(-1)复合右美托咪定0.05μg·kg~(-1)·h~(-1),背景输注速率2ml/h,每次按压0.5ml,锁定时间10min)。记录术后6、12、24和48h安静、运动和宫缩状态下的VAS评分;术后48h内产妇泌乳后取乳汁,采用高效液相色谱质谱联用法(HPLCMS/MS)测定乳汁中右美托咪定浓度并计算相对婴儿摄取量(RID);记录术后产妇满意度以及不良反应的发生情况。结果与C组比较,D组在术后6、12、24h安静、运动和宫缩状态下VAS评分明显降低(P0.05),D组在术后48h运动VAS评分明显降低(P0.05);D组产妇满意度明显高于C组(P0.05);D组右美托咪定RID值为(0.197±0.114)%;两组术后均未发生低血压、低氧血症、呼吸抑制、心动过缓以及恶心和呕吐等不良反应。结论健康产妇围术期使用右美托咪定可安全哺乳。术后镇痛使用布托啡诺复合0.05μg·kg~(-1)·h~(-1)右美托咪定能够提供满意的镇痛效果。     

左下肺癌切除术中肿瘤组织阻塞双腔管一例

患者,男,67岁,58 kg.因左下肺占位,拟行左下肺叶切除术.术前CT示左下肺癌伴纵隔淋巴结转移.肺功能检查示中度阻塞性通气功能障碍,轻度弥散功能障碍.其余检查无明显异常.麻醉前常规用药,依次静脉注射地塞米松10 mg、咪唑安定3 mg、依托咪酯18 mg、维库溴铵8 mg、芬太尼0.2 mg.插入左侧双腔气管导管(35#),深度27 cm.纤维支气管镜定位检查双腔管位置良好,纤维支气管镜下发现在气管隆突的位置有一个凸起的小肿块,性质不明,未予重视,行机械通气(f=10次/分,I:E=1:2,V_(T8)ml/kg).丙泊酚100 μg·kg~(-1)·min~(-1)、阿曲库铵8μg·kg~(-1)·min~(-1)、雷米芬太尼0.03μg·kg~(-1)·min~(-1)维持麻醉.     

垂体后叶素用于顽固性低血压合并肺动脉高压一例

患者,女,47岁,51 kg,因"风湿性心脏病,二尖瓣重度狭窄(二尖瓣口面积0.8cm2)"入院,拟行二尖瓣置换术.患者术前存在房颤,肺动脉高压(PH),平均肺动脉压力( MPAP)约41 mm Hg,NYHA和ASAⅢ级,心胸比为0.7.入室后建立静脉通道,常规监测ECG、IBP、SpO2.麻醉诱导:静注咪达唑仑0.05 mg/kg、依托咪酯0.1～0.2 mg/kg、维库溴铵0.15 mg/kg、芬太尼10 μg/kg.诱导后放置中心静脉导管、swan-ganz漂浮导管和经食管超声.麻醉维持:异氟醚0～2％、丙泊酚6～10 mg· kg-1·h-1、阿曲库铵5～10μg· kg-1 ·min-1,间断静脉推注芬太尼20μg/kg.CPB时间共99 min.     

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.     

重症监护病房护士工作体验的质性研究

目的 了解重症监护病房护士在临床工作中的真实感受,为护理管理者合理安排工作、及时满足护士需求提供参考.方法 2013年10-12月,运用质性研究中的现象学研究法,对解放军总医院重症监护病房的10名护士进行深度访谈,将获取的资料进行分析、总结,归纳形成主题.结果 整理形成10份完整的访谈资料,通过对访谈资料的反复提炼、分析和萃取,最终得出以下6个反映ICU护士工作体验的主题:休息不足、社会支持缺乏、工作环境复杂、薪酬较低、心理压力过大、自我发展空间局限.结论 护理管理者应深入了解并重视重症监护病房护士的工作体验,采取人性化管理模式,减轻其工作负荷与压力,及时满足其身心需求,疏导其不良情绪,从而提高工作效率,提升护理质量.