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.     

前列腺素E1治疗活动性消化性溃疡96例疗效观察

前列腺素Ｅ(ＰＧＥ)是花生四烯酸代谢产物 ,对机体各系统生理功能及物质代谢有明显调节作用 ,日益受到人们的重视。近几年来 ,我们使用前列腺素Ｅ1(ＰＧＥ1)冻干粉针 (规格 :10 0 μｇ/支 ) ,治疗活动性消化性溃疡取得较好疗效 ,现将结果报告如下。1　资料与方法1.1　临床资料     

老龄脑卒中长期卧床患者肺部感染状况及干预措施

目的 探讨老龄脑卒中长期卧床患肺脏长期保护措施。方法 回顾分析29例老龄脑卒中病卧肺炎相关因素、特点和死因。结果 多种综合干预仍可引起院内获得性肺内感染，且治疗不愈。结论 有效的肺保护技巧将使观念从仅重视救治成功率转换到肺脏的保护及疾病的预防上来。     

喉全切除术食管发音机制研究

目的 探讨喉全切除术后食管言语的特点。方法 对北京同仁医院40例训练食管发音患者的噪音声学、言语、形态特征及发音时食管压力变化进行分析。以50例健康男性作为对照。结果 食管发音不良8例，发音良好32例。发音不良黏膜痉挛，气流无法送出；发音基频小于60Hz无法评估。发音良好者食管人口黏膜松驰，振动明显；其噪音声学特征与健康对照差异有显著性（P值＜0．05或＜0．01）。食管发音不良者训练发音年龄、言语清晰度、速度、呼吸发音协调程度与发音良好者差异有显著性（P值＜0．05或＜0．01）。食管发音时食管上、中段压力明显高于健康对照组（P值＜0．05或＜0．01），其中发音不良者压力增加更为明显，特别是食管中段压力。结论 食管发音声道振动及动力器官均与正常发音存在本质区别，通过代偿机制瞬间发音可达良好效果，但在自然、持续言语交流中存在明显障碍。