羟考酮联合右美托咪定在老年患者下肢动脉闭塞支架置入手术中的应用

目的探讨羟考酮联合右美托咪定在老年患者下肢动脉闭塞(artriosclerosis obliterans, ASO)手术监测麻醉(monitored anesthesia care, MAC)的临床效果及安全性。方法选择2017年6月至2018年12月择期行下肢动脉闭塞介入手术治疗患者80例,男63,女17,年龄65～85岁,ASAⅡ或Ⅲ级,采用随机数字表法分为羟考酮联合右美托咪定组(O组,n=40)和芬太尼联合右美托咪定组(F组,n=40)。记录有创测压后患者平静呼吸5 min后(T_1)、股动脉穿刺置鞘时(T_2)、球囊扩张时(T_3)、手术结束时(T_4)的MAP、HR以及SpO_2;术中VAS、Ramsay评分、手术时间、出室时Ramsay评分。同时观察围术期不良反应。结果两组患者一般情况、下肢动脉硬化闭塞分级、手术时间和出室Ramsay评分差异均无统计学意义。与T_1时比较,T_2时两组MAP明显降低,HR明显减慢,且F组明显低于O组(P0.05)。T_3时F组VAS评分、Ramsay评分明显高于O组,术毕至出恢复室观察时间明显长于O组(P0.05)。术中体动反应、术中呼吸抑制以及术后恶心呕吐发生率F组明显高于O组(P0.05)。结论羟考酮联合右美托咪定可安全用于老年患者下肢动脉闭塞手术监测麻醉中,能够有效控制疼痛反应,提高手术舒适度,维持术中循环稳定,减少术中呼吸抑制发生率以及术后恶心呕吐发生率。     

Rh(D)阳性血用于Rh(D)阴性患者术中大出血抢救成功一例

患者,女,56岁,58kg,因"间断性右腰痛1月余"入院,诊断为"右肾上腺占位".患者一般情况良好,既往无输血史,生育史4-0-0-4.入院检查:BP 116/73mmHg,HR 72次/分.ECG正常;血型鉴定:O型,Rh(D)阴性;血生化和心肺肝肾功能检查均在正常范围;B超示肾上腺来源,腹膜后占位112mm×90 mm;血去甲肾上腺素9736.3 pg/ml,肾上腺素433.8 pg/ml;PET-CT示右肾上腺区巨大肿块伴囊性变及钙化,考虑为低度恶性肿瘤,皮质腺癌或嗜铬细胞瘤的可能.患者入院后给予酚苄明等术前准备,拟在全麻下行嗜铬细胞瘤切除术.     

达芬奇机器人辅助腹腔镜前列腺根治术后肺不张的临床分析

目的对达芬奇机器人辅助腹腔镜前列腺根治术后治疗的出现肺不张的患者进行临床分析,探究潜在的影响因素。方法利用血气分析仪测定患者手术前和拔管后的血气参数值并在超声下诊断肺不张。结果手术前动脉血中PaO_2分压和SaO_2高于拔管后,表明手术后患者中氧气浓度呈现下降(P0.05),而PaCO_2在拔管后出现了显著升高(P0.05)。同时拔管后的血气参数PaO_2和SaO_2与是否拔管后人工张肺存在正相关性,并与PaCO_2表现出负相关性(P0.05)。结论达芬奇机器人辅助腹腔镜前列腺根治术后的肺不张表现为动脉血氧浓度下降和二氧化碳升高,并且人工张肺有利于缓解肺不张的症状。     

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.     

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.     

HPLC测定骨筋丸片中龙胆苦苷的含量

目的:建立骨筋丸片定量检测方法。方法:高效液相色谱法(HPLC)。C18柱(150mm×4.6mm,5μm),流动相:甲醇-水(1∶3),流速1.0ml/min,检测波长254nm。结果:龙胆苦苷进样量0.05～0.80μg与峰面积呈良好的线性关系(r=0.9997),回收率为98.85%,RSD为1.16%。结论:该法操作简便、准确,可作为骨筋丸片中的含量测定方法。     

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.     

机器人辅助腹腔镜前列腺癌根治术经腹膜途径和腹膜外途径术后肺不张观察

应用肺部超声技术比较经腹膜途径机器人辅助腹腔镜前列腺癌根治术（transperitoneal robot-assisted laparoscopic radical prostatectomy, T-RLRP）和腹膜外途径机器人辅助腹腔镜前列腺癌根治术（extraperitoneal robot-assisted laparoscopic radical prostatectomy, E-RLRP）术后肺不张情况。 方法 采用随机数字表法将40例患者分为T-RLRP组和E-RLRP组,每组20例。两组患者分别于麻醉前（T0）,建立气腹和Trenderlenburg体位后60 min（T1）、120 min（T2）和气管拔管后（T3）,抽取桡动脉血,观察PaO2/FiO2和PaCO2;记录气腹和Trenderlenburg体位后120 min内的平均气道压;术毕拔管前,肺部超声下观察患者肺不张程度。 结果 术中T-RLRP组的平均气道压高于E-RLRP组（P＜0.05）。T-RLRP组PaO2/FiO2水平T1和T2时点明显低于T0水平（P＜0.05,P＜0.01）,T2时点低于T1时点水平（P＜0.05）。E-RLRP组在T2时PaO2/FiO2水平低于T0（P＜0.05）,T1、T2和T3时点PaO2/FiO2水平均明显高于T-RLRP组（P＜0.01,P＜0.05,P＜0.05）。两组T1和T2时点PaCO2明显高于T0（P＜0.01）,T-RLRP组T1和T2时点PaCO2均高于E-RLRP组（P＜0.05）。术毕肺部超声显示肺不张1级、2级和3级,T-RLRP组比例均明显高于E-RLRP组（P＜0.01）。 结论 相比T-RLRP组,E-RLRP对患者术中和术后氧合影响更小,术后肺不张发生程度更轻。     

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.