手术结束前应用地氟醚替换异氟醚对麻醉苏醒及花费的影响

目的 探讨手术结束前30 min应用地氟醚替换异氟醚对患者麻醉苏醒的影响。方法 选取2016年4月~2017年4月择期妇科腹腔镜手术患者90例,ASAⅠ~Ⅱ级,随机分为D组（地氟醚）、I组（异氟醚）和I+D组（异氟醚+地氟醚）三组,每组30例。全麻诱导均为咪达唑仑0.03 mg/kg,舒芬太尼0.3 μg/kg,异丙酚2 mg/kg,顺式阿曲库铵0.15 mg/kg。麻醉维持:D组开启地氟醚挥发罐至6%;I组开启异氟醚挥发罐至1.6%;I+D组开启异氟醚挥发罐至1.6%,手术结束前30 min关闭异氟醚,同时开启地氟醚挥发罐至6%,三组均复合瑞芬太尼0.1~1 μg/（kg·min）维持麻醉。手术结束停用所有麻醉药,观察呼吸恢复时间、苏醒时间、拔除喉罩时间、苏醒期躁动评分和术中知晓,计算三组用药量及花费。结果 D组和I+D组的呼吸恢复时间、苏醒时间、拔除喉罩时间均比I组缩短,差异有统计学意义（P＜0.05）;两两比较:D组和I+D组间差异无统计学意义（P＞0.05）,其余两两比较结果均有统计学意义（P＜0.05）。三组间苏醒期躁动评分差异无统计学意义（P＞0.05）。I+D组麻醉药花费较D组减少,差异有统计学意义（P＜0.05）。结论 手术结束前应用地氟醚替换异氟醚可加快患者麻醉苏醒且花费相对较低。     

RAGE阻断剂FPS-ZM1减轻异氟醚麻醉诱发老龄大鼠认知功能障碍

目的探讨RAGE阻断剂FPS-ZM1对异氟醚麻醉诱发老龄大鼠认知功能障碍的影响。方法将老龄大鼠60只,随机分为4组(n=15):NS+O2组、NS+ISO组、FPS-ZM1+ISO组及FPS-ZM1+O2组。NS+O2组及NS+ISO组,侧脑室注射无菌0.9%氯化钠溶液10μL,FPS-ZM1+ISO及FPS-ZM1+O2组,侧脑室注射FPS-ZM1 10μL(5 g/L)。侧脑室注射后24 h,NS+O2及FPS-ZM1+O2组吸入含有30%氧气的空氧混合气体4 h,FPS-ZM1+ISO及FPS-ZM1+ISO组吸入2%异氟醚+100%氧气4 h。用Morris水迷宫评测大鼠学习和记忆功能,用免疫组织化学技术观察海马CA1区RAGE及Aβ的表达。结果与NS+O2组相比,NS+ISO组第1~4天逃避潜伏期延长、探索时间缩短、海马CA1区RAGE表达上调、Aβ表达上调。与NS+ISO组相比,FPS-ZM1+ISO组第1~4天逃避潜伏期缩短,探索时间延长,RAGE表达下调、Aβ表达下调。结论 RAGE阻断剂FPS-ZM1可改善异氟醚麻醉诱发老年大鼠认知功能障碍,其机制可能与其抑制海马CA1区Aβ沉积有关。     

异氟醚对成年大鼠行为学的影响

目的探讨国产异氟醚（宁芬）对成年大鼠学习记忆功能的影响。方法成年雄性SD大鼠36只（n=6×6组）,将其随机分为空白对照组（A组）、阳性对照组（02组）、麻醉组。三组大鼠进行Morris水迷宫定位航行适应性训练5d,记录逃避潜伏期和总路程。麻醉组吸人2．0％浓度国产异氟醚30min,苏醒后2h、1d、7d、14d再次行水迷宫实验,观察指标与适应性训练相同。结果麻醉30min呼吸次数明显减少;与第1天比较,第2,3、4,5天逃避潜伏期、总路程差异显著（P〈0．01）,且随着天数的增加逐渐缩短。结论大鼠吸入宁芬30min后,1d内对学习记忆有一定程度影响,1d后学习记忆逐渐改善,自行恢复到麻醉前水平。     

丙泊酚和七氟醚对老年患者术后认知功能障碍的影响

目的比较丙泊酚和七氟醚对老年患者术后早期认知功能的影响。方法筛选年龄≥65岁,ASAⅠ~Ⅱ级的患者62例行择期胸腹部手术,随机分为丙泊酚组和七氟醚组,每组31例。患者术前及术后6 h、12 h、24 h和48h均采用MMSE评价认知功能。结果术后6h、12h、24h丙泊酚组和七氟醚组MMSE评分比较,差异显著(P<0.05),且随时间的延长,POCD得到改善,术后48 h ,基本恢复正常。结论丙泊酚和七氟醚均可降低老年患者术后早期的认知功能,但七氟醚比丙泊酚认知功能恢复快。     

七氟醚麻醉对食管癌手术患者脑氧代谢及认知功能的影响

目的:探讨七氟醚麻醉对食管癌手术患者脑氧代谢及认知功能的影响.方法:回顾性分析2018年4月至2019年4月我院收治的79例食管癌手术患者临床资料,按照麻醉方案不同进行分组,其中采用丙泊酚麻醉的38例为对照组,采用七氟醚麻醉的41例为观察组.观察术后两组恢复指标(呼吸恢复时间、气管拔管时间及定向力恢复时间)及麻醉前(T...     

七氟醚与异氟醚分别复合氧化亚氮全程吸入麻醉的临床应用

目的观察七氟醚与异氟醚分别复合氧化亚氮在紧闭式静吸复合全麻中的临床应用。方法选择60例ASAⅠ-Ⅱ级择期手术患者,随机分为S、I两组,每组患者均于诱导前静注咪唑安定004mg／kg＋太尼2ug／kg,1分钟后S组吸入5％七氟醚＋50％氧化亚氮,Ⅰ组吸入3％异氟醚＋50％氧化亚氮,待患者入睡后静注罗库溴铵06mg／kg,气管插管后S组继续吸入1．0-30％七氟醚＋50％氧化亚氮,I组吸入0．6～18％异氟醚＋50％氧化亚氮至术毕,同时观察各时点MAP、HR、SPO2、。BIS及吸入麻醉药浓度,手术结束观察病人苏醒及拔管时间,术后随访术中知晓、恶心、呕吐及有无其它不良反应。结果七氟醚与异氟醚分别复合氧化亚氮全程吸入麻醉,结合BIS监测指导术中用药,使诱导、苏醒迅速,麻醉过程平稳,麻醉深度易控制,对患者血流动力学影响小。结论七氟醚与畀氟醚分别复合氧化亚氮全程吸入麻醉是一种安全有效的麻醉方法,可作为临床麻醉用药的另一种选择。     

七氟醚和异氟醚低流量麻醉用于腹腔镜手术的比较

目的：在腹腔镜手术中采取七氟醚低流量麻醉和异氟醚低流量麻醉,观察两组应用效果。方法选取我院收治的行腹腔镜手术患者56例,按照分层随机法,随机分为I组合II组,I组采取七氟醚低流量麻醉,II组采取异氟醚低流量麻醉,比较两组应用效果。结果 I 组患者气腹前SBP、DBP及HR在T2、T3、T4时与I组比较,差异有统计学意义(P<0.05)。I 组苏醒时间及拔管时间均长于I组,有显著性差异(P<0.05)。结论七氟醚血流动学更平稳,是一种安全可靠的麻醉方法。     

生长抑素Ⅳ型受体激动剂改善异氟醚麻醉所致老年大鼠认知功能障碍

目的探讨生长抑素Ⅳ型受体激动剂(NNC 26-9100)对异氟醚麻醉所致老年鼠学习记忆障碍的改善作用。方法将20月龄老年SD大鼠随机分为4组(n=14):对照组、异氟醚组、异氟醚+药物组和单纯药物组。异氟醚+药物组和单纯药物组侧脑室注射NNC 26-9100,而对照组和异氟醚组注射等量溶媒。24 h后异氟醚组和异氟醚+药物组吸入2%异氟醚4 h,而对照组和单纯药物组吸入纯氧4 h。通过Morris水迷宫检测记忆能力、real-time PCR和Western blot检测中性内肽酶(NEP)和胰岛素降解酶(IDE)在海马区表达。结果与异氟醚组相比,异氟醚+药物组大鼠第2天及第3天逃避潜伏期缩短(P0.05),目的象限探索时间延长(P0.05)。各组海马区NEP和IDE在mRNA及蛋白水平两两比较均无显著差异。结论生长抑素Ⅳ型受体激动剂(NNC-9100)可显著改善异氟醚麻醉所致老年鼠学习记忆障碍。     

异氟醚麻醉对脑内ERK1/2和PKCγ磷酸化水平的影响

目的:探讨异氟醚麻醉对脑内ERK1/2和PKCγ磷酸化水平的影响.方法:采用雄性BALB/c小鼠, 随机分为5组, 即对照组(Con):未麻醉;异氟醚麻醉5 min组(Iso-1);异氟醚麻醉1 h组(Iso-2);麻醉1 h后停药2 min组(E-1):异氟醚麻醉1 h后, 小鼠脱离麻醉环境2 min;麻醉1 h后停药1 h组(E-2):异氟醚麻醉1 h后, 小鼠脱离麻醉环境1 h.用异氟醚进行麻醉后进行Western blot.以β-Actin为内参, pERK A/Actin A为ERK表达水平指标, pPKCγ A/Actin A为pPKCγ表达水平指标.结果:在Con组, pERK1/2和pPKCγ呈现高表达状态, 给予异氟醚麻醉处理组(Iso-1和Iso-2组), pERK1/2和pPKCγ表达减弱(P＜0.05), 当异氟醚麻醉停止后(E-1和E-2组), pERK1/2和pPKCγ表达逐渐恢复, 与Con组相比无统计学差异, 与异氟醚处理组相比, 有统计学差异(P＜0.05).结论:异氟醚麻醉-苏醒过程中, 脑中部分核团pERK1/2和pPKCγ水平发生显著变化.     

安氟醚和异氟醚预处理对实验小鼠肝组织Bcl-2/Bax mRNA和蛋白表达的影响

目的:探讨吸入异氟醚和安氟醚预处理对实验小鼠肝组织Bcl-2和Bax基因和蛋白表达的影响。方法:120只C57BL/6小鼠随机分成安氟醚预处理组(E组)和异氟醚预处理组(I组),每组60只;各组又分为麻醉前(T0)、麻醉即刻(T1)、麻醉2h(T2)、麻醉4h(T3)、麻醉6h(T4)和麻醉终止后2h(T5)。取两组各时相肝组织检测Bcl-2和Bax mRNA及蛋白表达水平。结果:两组Bcl-2 mRNA及Bcl-2和Bax蛋白水平在T1表达均有所下调,但差异无统计学意义(P>0.05);在T2～T5表达上调(P<0.05或P<0.01),并随麻醉时间延长而逐渐增加,即T4时上调最明显(P<0.01);麻醉停止后(T5)开始恢复。两组Blc-2蛋白水平在T2～T5均较T0时增加,而Bax蛋白在T3～T5时增加(P<0.05或P<0.01);两组Bcl-2/Bax蛋白比值与T0时相比,E组在T1～T3、I组在T1～T5均明显升高(P<0.05)。结论:吸入安氟醚、异氟醚后肝组织Bcl-2和Bax表达增加,以Bcl-2更为明显;安氟醚、异氟醚预处理保护肝脏的作用可能与其抑制肝细胞凋亡有关。     

Environmental influences on cognitive decline in aged rats

Two experiments are reported in which young and old rats, housed in an impoverished (IE), enriched, (EE), or standard (SE), environment, were tested on a series of complex, blind-alley mazes. In Experiment 1, 3-months exposure to IE exacerbated age differences in maze performance, relative to the differences between young and old rats in EE and SE. Old rats in the EE and SE conditions did not differ from each other. In Experiment 2, rats were raised for an additional 3 months in either IE or EE before further maze testing. The main findings were that the maze performance of old rats, transferred from IE to EE, improved significantly, whereas the performance of old rats, transferred from SE or EE to IE, declined. These results indicated that the deleterious effects of an impoverished environment on learning and memory are, at least partly, reversible, and that experience in a stimulating environment can protect old rats from the adverse effects of relocation to a deprived environment. Taken together, the results highlight the impact of environmental influences on cognitive function in old age, and emphasize the need to consider nonbiological factors in understanding the process of cognitive aging.     

全麻气管插管后七氟醚和异氟醚吸入对吸烟患者呼吸力学的影响

目的 比较观察全麻气管插管后七氟醚和异氟醚吸入对吸烟和非吸烟患者气道阻力、肺顺应性和气道峰压的影响.方法 选择既往有和无吸烟史择期手术的普通外科患者80例[美国麻醉医师协会(ASA)Ⅰ～Ⅱ级,既往有或无吸烟史患者各40例],随机分为4组(n=20):有吸烟史患者吸入七氟醚全麻组(SS组)和吸入异氟醚全麻组(SI组),无吸烟史患者吸入七氟醚全麻组(NS组)和吸入异氟醚全麻组(NI组).使用多功能麻醉气体监护仪监测患者吸入麻醉剂浓度达到肺泡最低有效浓度(1MAC)后4、8、12、16min的气道峰压、肺顺应性,同时用无创心功能测定仪监测气道阻力,记录各组患者在吸入麻醉剂期间各项指标的变化情况.结果 与吸入前相比,所有接受全麻气管插管的患者在使用七氟醚和异氟醚吸入维持4、8、12、16 min后均出现气道阻力和气道峰压的明显下降(均P＜0.05),其中SS组和NS组8min后下降趋于稳定[气道阻力:SS组(10.38±1.12)cmH2O·L-1·s-1,NS组(9.65±1.04)cm H2O·L-1·s-1;气道峰压:SS组(13.52±1.01)cm H2O,NS组(12.86±0.94)cm H2O,1 cm H2O=0.098kPa],SI组和NI组则于12 min后下降趋于稳定[气道阻力:SI组(10.30±0.98)cm H2O·L-1·s-1,NI组(11.00±0.73)cm H2O·L-1·s-1;气道峰压:SI组(13.47±0.88)cm H2O,NI组(12.85±0.65)cm H2O],同时间点的非吸烟组下降幅度高于吸烟组(均P＜0.05).4组患者在使用七氟醚和异氟醚吸入维持后其肺顺应性较吸入前均无明显变化(均P＞0.05),同时间点的非吸烟组与吸烟组相比肺顺应性差异也没有统计学意义(均P＞0.05).结论 全麻气管插管后七氟醚和异氟醚吸入使患者的气道阻力和气道峰压出现明显下降,吸烟者比非吸烟者下降程度低.     

ProNGF-p75~(NTR)在异氟醚暴露的老年小鼠认知功能下降中的作用

目的:探讨神经生长因子前体(pro NGF)与其受体p75~(NTR)特异性结合(pro NGF-p75~(NTR))在异氟醚暴露的老年小鼠认知功能障碍中的作用。方法:30只C57BL/6J雄性老年小鼠随机分成3组:正常(control)组、异氟醚(Iso)组和p75~(NTR)抑制剂2-氨基-3-甲基-戊酸酰胺(LM11A-31,LM)+异氟醚(LM+Iso)组。各异氟醚处理组的小鼠每天吸入1%异氟醚3 h,连续7 d;control组每天吸入空气3 h,连续7 d。LM溶于无菌生理盐水,在吸入异氟醚之前按50 mg·kg-1·d-1的剂量对LM+Iso组老年小鼠进行灌胃,连续1个月;control组和Iso组小鼠仅给予同等体积的生理盐水。用动脉血气分析法监测异氟醚暴露后小鼠生理状态。Morris水迷宫实验观察小鼠行为学的改变。Western blot检测各组小鼠海马组织中pro NGF、p75~(NTR)、磷酸化p38 MAPK和cleaved caspase-3蛋白水平的变化。结果:与control组比较,Iso组海马组织中pro NGF和p75~(NTR)的蛋白表达水平显著增加(P0.05)。Iso组海马组织中p38 MAPK的磷酸化水平较control组显著升高(P0.05);LM+Iso组p38 MAPK的磷酸化水平较Iso组显著下降(P0.05)。Iso组海马组织中cleaved caspase-3的蛋白水平较正常组显著升高(P0.05),而LM11A-31干预可以明显下调异氟醚诱导小鼠海马组织中cleaved caspase-3的蛋白水平(P0.05)。与control组相比,Iso组小鼠找寻平台的潜伏期明显延长(P0.05),小鼠穿越原平台次数减少(P0.05);而LM+Iso组小鼠的逃避潜伏期较Iso组小鼠显著缩短(P0.05),穿越原平台次数较Iso组小鼠增加(P0.05)。结论:Pro NGF-p75~(NTR)可能在异氟醚暴露的老年小鼠凋亡信号通路的活化以及认知功能的下降过程中起一定作用,这为临床干预提供了潜在的靶点。     

Postsynaptic depression induced by isoflurane and Althesin in neocortical neurons

Summary The effects of two general anaesthetics, isoflurane — a volatile agent, and Althesin — a steroid preparation, were studied on the membrane electrical properties and spike activities of 64 neurons in in vitro slice preparations of neocortex excised from anterior cingulate and sensorimotor areas of guineapig brain. Spontaneous activity was depressed, and the thresholds for spikes evoked by intracellular injections of current pulses were increased in most neurons during applications of isoflurane in clinical concentrations (0.5–2.5 minimum alveolar concentration or MAC) and Althesin (15–100 M). The MAC values are equivalent to 1–4% isoflurane in the gaseous phase. Applications in the higher ranges (1.5–2.5 MAC and 300–1500 M) usually induced a small hyperpolarization (range, 3–8 mV) and an increase (10–30%) in input conductance. The repetitive spike firing evoked by current-pulse injections was inhibited and not uncommonly, abolished completely by an anaesthetic application. A striking feature in the actions of both agents on all neurons was the dose-dependent, reversible depression in amplitude and duration of the postspike afterhyperpolarizations (AHPs). These effects could not be attributed to anaesthetic induced changes in resting potentials, input conductances, or to the reduced number of evoked spikes. Bicuculline (50 M) was applied concomitantly in 8 neurons with the anaesthetics to block Cl-conductances mediated by GABA-receptors that otherwise may contaminate the AHPs. In the presence of bicuculline, both anaesthetics produced a greater reduction in the amplitude and duration of the AHPs which are generated through Ca²⁺-mediated K⁺-conductance. The changes in input conductance induced by Althesin were partially blocked by bicuculline indicating that endogenous actions of GABA contributed to the effects of Althesin. These investigations have shown that isoflurane and Althesin attenuate the excitabilities of neocortical neurons by postsynaptically depressing the medium-duration AHPs and thereby decreasing their abilities to fire spikes repetitively. It is concluded that these effects produced by anaesthetic administration would result in a disruption in the organized pattern of neocortical arousal.     

A non-invasive intranasal inoculation technique using isoflurane anesthesia to infect the brain of mice with rabies virus

Methods for intranasal inoculation of viruses are often described poorly and the effects of variations in the technique on the outcome are unknown. Standardization of protocols is key to compare studies and minimize animal use. The clinical and virological outcome of infection with rabies virus (genotypes 1 and 5) upon administration of different inoculum volumes (25, 50 and 100 μl) and different anesthetic regimens were examined. Administration of 25 μl of virus as a drop on both nostrils under brief superficial isoflurane anesthesia (92 μl/dm³, recovery after 85 ± 10 s) was the most effective to infect the brain and induced 100% lethal infection 9 days later. Increasing the inoculum volume reduced infectivity significantly, with decreased viral loads in the brain and only 40% mortality. Increasing the depth of isoflurane anesthesia (230 μl/dm³) improved the infectivity of the large-volume inoculum (90% mortality), probably because of suppression of swallow and sneeze reflexes. Compared to isoflurane anesthesia, xylazine-ketamine anesthesia reduced the infectivity of the inoculum significantly. Thus, administration of a small volume of virus on the nostrils under brief gas anesthesia is a safe and reproducible technique to induce infection of the brain. Since needles are not required, this helps to preserve the integrity of the physical barriers, animal welfare and the manipulator's safety.     

丙泊酚麻醉对老年大鼠记忆功能影响的行为学研究

目的：研究丙泊酚麻醉对老年大鼠认知功能的影响。方法选取96只雄性SD老年大鼠（16月龄）为研究对象,在丙泊酚麻醉后第7、30、90天,应用恐惧记忆实验测试老年大鼠长期记忆功能（每个时间节点各12点,共36只）;在麻醉后5 d内应用自主空间探索实验测试老年大鼠工作记忆功能（每个时间节点各12点,共60只）。结果在麻醉后7、30、90 d,丙泊酚组与对照组老年大鼠长期记忆功能的差异均无统计学意义（P>0.05）。麻醉后2 d内,丙泊酚组老年大鼠工作记忆功能受损（P<0.05）;在第3、4、5天,2组老年大鼠空间工作记忆差异均无统计学意义（P>0.05）。结论实验结果表明临床剂量丙泊酚麻醉会导致老年大鼠48 h内的工作记忆功能损伤,但不会损伤其长期记忆功能。     

TREK1 activation mediates spinal cord ischemic tolerance induced by isoflurane preconditioning in rats

The aim of this study is to examine the role of one of the two-pore (2P) domain K⁺ channels, TREK (TWIK-related K⁺ channels, TREK)-1, mediated neuroprotection on spinal cord afforded by isoflurane preconditioning. In Experiment 1, male Sprague-Dawley rats were randomly assigned to control (Con) group, an iso?urane preconditioning (Iso) group, and sham group. Twenty-four hours after the last pretreatment, spinal cord ischemia was induced in Con and Iso groups. Neurobehavioral testing and histopathologic examination were performed after reperfusion. In Experiment 2, the expression of the TREK1 in the spinal cord was assessed by immunohistochemistry, Western blot and real-time polymerase chain reaction. In Experiment 3, Amiloride, a blocker of stretch-sensitive channels, was administered intraperitoneally immediately prior to each isoflurane preconditioning. Iso group showed a significant reductions in motor deficit index as well as increases in the number of normal neurons compared with the Con group. The expression of TREK1 protein and the level of mRNA after ischemia were higher in the rats of the Iso group than those in the Con group. Amiloride pretreatment abolished the protective effects of Iso preconditioning. These finding indicate that isoflurane preconditioning had a neuroprotective effect against spinal cord ischemia reperfusion injury. These effects may be mediated through the TREK1 pathway.