氟烷和氟醚类麻醉剂诱导c-fos基因在间脑部分核团的表达

本研究旨在了解氟烷和氟醚类吸入麻醉剂在间脑的作用部位. 大鼠分别吸入2％甲氧氟烷, 氟烷, 安氟醚和异氟醚麻醉1 h, 应用免疫组织化学法, 光镜观察Fos蛋白阳性神经元在间脑的分布并计数. 研究提示在吸入麻醉过程中间脑有15个神经核团呈现Fos阳性, 分别是丘脑室旁核, 丘脑中央中核, 丘脑再连合核, 菱形丘脑核, 背外侧膝状核, 背内侧梨状核, 丘脑背外侧核, 丘脑后外侧核, 下丘脑室周核, 视前中核, 视上核, 弓状核, 视交叉上核, 丘脑腹后外侧核和缰核. 结果表明吸入氟烷和氟醚类麻醉剂在间脑具有明确的作用位点, 而不是弥散性的.     

安氟醚和异氟醚对手术中急性心肌缺血的影响

目的 :评价安氟醚和异氟醚对手术中急性心肌缺血患者心电图和血压的影响。方法 :43例ASAⅡ～Ⅲ级手术患者 ,按治疗药不同分成3组 ,A组15例用硝酸甘油、B组14例用安氟醚 ,C组14例用异氟醚。其中硬膜外麻醉15例(占34.9%) ,麻醉药为利多卡因 ;全身麻醉28例(占65.1 %) ,麻醉诱导药安定、氟芬合剂、羟基丁酸钠、丙泊酚和琥珀胆碱。麻醉维持药芬太尼加维库溴铵间断静注 ,同时复合吸入0.1～0.5MAC(肺泡气最低有效浓度)安氟醚或异氟醚。治疗A组硝酸甘油1～5μg·kg-1·min -1、B组1.5～2.5MAC安氟醚、C组吸入与B组相同浓度的异氟醚。硬膜外麻醉先静注氟哌啶醇2.5mg和哌替啶50mg,然后吸入安氟醚或异氟醚 ;全身麻醉则直接加大该两药的吸入浓度。采用t检验 ,比较治疗前后心率(HR)、心电波S-T段、肱动脉平均压(MBAP)和心率收缩压乘积(RPP)的变化值。结果 :除MBAP外 ,A组与B组和C组比较 ,各项均有显著性差异(P<0.01) ,而在降低HR和RPP上 ,B组与C组比较又有显著性差异(P<0.01)。结论 :安氟醚和异氟醚在迅速改善术中急性心肌缺血的心电波和血压上优于硝酸甘油 ,而安氟醚在降低RPP上又优于异氟醚。     

地氟醚、异氟醚实施循环紧闭麻醉的临床比较

目的　比较地氟醚与异氟醚在循环紧闭麻醉的临床效果及效能价格比。方法　 30例择期手术病人 ,分为地氟醚组 (D组 )、异氟醚组 (I组 ) ;麻醉诱导用咪唑安定、芬太尼和琥珀胆碱。气管插管后最初氧流量为 4L/ min,挥发罐浓度 D组、 I组设于 8%和 2 % ,在呼气末浓度分别达 6 %、 1.1%后关闭回路 (氧流量为 0 .2 0～ 0 .35 L / min)行循环紧闭麻醉。D组和 I组 FD调整至 12 %和 4% ,术中维持地氟醚 FA 于 6 %± 0 .1% ,异氟醚 FA 于 1.1%± 0 .1% ;手术结束前 10分钟关闭发挥罐 ,手术后开放回路 ,氧流量 4L/ min,术中予维库溴胺维持肌松。结果　在循环紧闭麻醉中地氟醚的费用比异氟醚便宜约 2 0 %。高流量诱导期 D组和 I组的时间分别为 4.9± 0 .8分和 7.5± 0 .4分 ,微流量后 30分FA/ FI 分别为 90 %和 73%。麻醉结束后地氟醚、异氟醚的 FA 下降至高流量洗出初始时肺泡浓度 FAO的 5 0 %时间分别为1.2± 0 .1分和 1.8± 0 .3分 ,拔管时间、拔管后整体恢复时间 D组明显短于 1组。结论　地氟醚在循环紧闭麻醉中的药代动力学、临床效果及效能价格比明显优于异氟醚     

七氟醚异氟醚和安氟醚麻醉苏醒的对比观察

为了比较七氟醚、异氟醚和安氟醚麻醉后的苏醒特征,将36例择期开胸手术病人均分为三组,用快速肺泡冲洗法分别测定各药物的初醒和完全清醒MAC,并系统观察临床苏醒过程。结果,七氟醚的初醒和完全清醒MAC为0.37±0.08％和0.26±0.06％;异氟醚为0.32±0.04％和026±0.04％;安氟醚为0.37±0.04％和0.31±0.05％。初醒和完全清醒时间七氟醚为5.0±1.9min和8.3=1.7min;异氟醚为8.9±2.6min和12.9±3.0min;安氟醚为9.6±2.9min和15.4±5.1min。显示尽管三种药的停药前维持浓度依次降低,但苏醒时间则依次延长,表明七氟醚的苏醒确实更快。另外发现术后三组病人均对初醒时的情景无明确记忆,完全清醒后还有3～5min的遗忘期。     

小儿全麻诱导吸入七氟醚和异氟醚的临床研究

目的比较七氟醚和异氟醚用于儿童患者全麻时的诱导，评估其安全性和麻醉效果。方法选择50例需全麻插管麻醉下行择期手术的患儿，随机分为七氟醚组和异氟醚组。所有患儿均不给术前药，人手术室后面罩分别直接吸人七氟醚或异氟醚复合纯氧（1-2L·min^-1），直至患儿睫毛反射消失，所有患儿均行气管插管，可合用阿曲库铵0．6mg·kg^-1保证肌松。结果诱导成功率均为100％，七氟醚组患儿睫毛反射和疼痛反应消失的时间明显短于异氟醚组（P〈0．01）。且不良反应较轻。结论小儿使用高浓度七氟醚的吸入诱导平稳而快速，与用异氟醚相比，睫毛反射消失时间和疼痛反应消失时间均明显缩短，麻醉满意，安全可控。     

七氟醚与异氟醚吸入用于腹腔镜胆囊切除术麻醉效果比较

目的比较七氟醚和异氟醚用于腹腔镜胆囊切除术麻醉效果。方法42例腹腔镜胆囊切除术患者随机分为七氟醚组（S组）和异氟醚组（Ⅰ组）,每组21例。快速诱导后麻醉维持两组分别吸入1MAC七氟醚和异氟醚,必要时追加芬太尼、罗库溴铵维持麻醉。记录诱导前（T0）、插管后5min（T1）、切皮（T2）、气腹开始（L）、缝皮（T4）、睁眼（T5）和拔管前（T6）,患者的HR、SP、DP和SpO2。计算从停止吸入麻醉药到睁眼和拔管的时间。结果1MAC七氟醚和异氟醚对病人血流动力学指标的影响均较轻,组间比较差异无统计学意义,S组患者的睁眼时间和拔管时间均比I组短,组间比较差异具有统计学意义。结论七氟醚和异氟醚吸入麻醉对腹腔镜胆囊切除术患者心血管功能的影响程度相似,但七氟醚全麻患者苏醒时间和拔管时间均明显短于异氟醚全麻患者。     

用七氟醚和异氟醚维持麻醉对吸烟者气道反应性影响的观察

目的探讨在异丙酚诱导以后用七氟醚和异氟醚进行诱导后吸烟者的气道副反应的发生率。方法选择40例ASA为Ⅰ～Ⅱ级17～75岁的每天吸烟支数不少于3支拟在全麻下进行手术病人,用异丙酚2～3mg/kg的静脉注射诱导后随机分配为两组:异氟醚组采用异氟醚维持麻醉,七氟醚组采用七氟醚维持麻醉。记录在麻醉维持过程中的气道副反应发生情况。结果吸烟者采用七氟醚进行诱导的副反应发生率10%,而异氟醚进行麻醉维持的副反应的发生率为45%(P<0.05)。结论全麻病人在用异丙酚静脉麻醉诱导后,用七氟醚维持麻醉较异氟醚维持麻醉具有更低的气道副反应的发生率,值得临床推广。     

异氟醚与七氟醚对老年人麻醉后苏醒和认知的影响

目的：比较异氟醚与七氟醚对老年人麻醉后苏醒和认知的影响。方法：选取择期行腹部手术的老年患者80例,随机分为异氟醚组（n=40）和七氟醚组（n=40）。记录患者的一般情况;监测手术后苏醒时间和拔管时间;测定患者简易智力状态检查（MMSE）评分。结果：两组患者的年龄、性别、手术时间以及输液量差异无统计学意义。七氟醚组患者的手术后苏醒时间和拔管时间明显短于异氟醚组,两组患者MMSE评分差异无统计学意义。结论：七氟醚麻醉后苏醒较异氟醚快,但两者对麻醉后老年患者认知能力没有明显影响。     

七氟醚与异氟醚用于婴幼儿唇腭裂修复术的麻醉效果比较

目的 观察比较七氟醚或异氟醚用于婴幼儿唇腭裂修复术的麻醉效果.方法 选择ASA Ⅰ ～Ⅱ级的择期行唇腭裂修复术的婴幼儿100例,将其随机分为两组:S组(七氟醚组,50例)采用七氟醚维持全身麻醉；Ⅰ组(异氟醚组,50例)采用异氟醚维持全身麻醉.观察两组患儿停药至苏醒时间、气管拔管时间、完全清醒时间及苏醒期并发症的发生率；并记录两组患儿的Fa/Fi及术后24 h的肌酐与尿素氮水平.结果 S组苏醒、拔管及清醒时间较Ⅰ组明显缩短(P＜ 0.05),苏醒期并发症较Ⅰ组明显减少(P＜0.05).S组20 min内的Fa/Fi明显高于Ⅰ组(P＜0.05),术后24 h两组的肌酐及尿素氮水平无明显差异(P＞0.05).结论 婴幼儿唇腭裂修复术中采用七氟醚麻醉较异氟醚麻醉苏醒更快且更安全.     

七氟醚与异氟醚两种吸入剂用于腹腔镜胆囊手术的麻醉恢复比较

目的 比较腹腔镜胆囊切除(LC)手术患者吸入七氟醚与异氟醚麻醉恢复的情况.方法 20例ASAⅠ-Ⅱ级择期行LC术患者随机分为两组,七氟醚组(A组)和异氟醚组(B组),各10例.麻醉诱导后行气管插管后机械通气.诱导后吸入纯氧,氧流量2 L/min.吸入七氟醚或异氟醚维持麻醉.维持血压和心率波动幅度不超过基础值30％,术中以盐酸瑞芬太尼微量泵静脉泵入.胆囊取出后停止吸入七氟醚或异氧醚,纯氧流量调整为6L/min.记录睁眼时间(停止吸入麻醉药到睁眼的时间)、记录拨除气管导管时间(停止吸入麻醉药到拔除气管导管时间)、记录麻醉后恢复期评分达到9分时间(从停止吸入麻醉药即刻计时).结果 与B组比较,A组睁眼时间、拨除气管导管时间、麻醉后恢复期评分达9分时间都较B组短.结论 在LC手术中,与异氟醚比较,吸入七氟醚患者麻醉恢复较快,且麻醉恢复质量较好.     

异氟烷和七氟烷对缺血神经元c-fos蛋白表达的影响和保护作用

目的　了解吸入麻醉药异氟烷和七氟烷对脑缺血神经元c fos蛋白表达的影响和保护作用。方法　用苏木素 伊红 (HE)染色法检测大鼠脑缺血梗塞体积和海马结构CA1～CA4亚区神经元损伤程度。用免疫组化法检测海马结构c fos蛋白的表达。结果　缺血 1h再灌 72h异氟烷组和七氟烷组脑梗塞体积显著小于缺血组 ;海马CA3和CA4亚区神经损伤程度也显著小于缺血组。缺血 1h再灌 4h ,在海马齿回 ,CA4亚区c fos蛋白样免疫反应率 ,吸入麻醉药组明显低于未吸入组。结论　异氟烷和七氟烷对缺血神经元有一定的保护作用。它们对c fos蛋白表达的衰减作用可能与其拮抗NMDA受体性质有关     

General anesthetics inhibit the nitrous-oxide-induced activation of corticotropin releasing factor containing neurons in rats

The activation of intracerebral corticotropin releasing factor (CRF) system is involved in nitrous oxide analgesia. We evaluated the effect of general anesthetics on nitrous-oxide-induced CRF activation and antinociception. Male Sprague-Dawley rats inhaled isoflurane (0%, 0.6%, 1.0% and 1.5%) or were administered with intravenous propofol (0, 0.1 and 0.2 mg/kg/min), with or without 75% nitrous oxide inhalation, for 90 min. The brain was fixed with fixative, and brain sections, including the paraventricular nucleus of the hypothalamus, were double immunostained with c-Fos and CRF antibodies to assess the activation of CRF-containing neurons. In other groups of rats, the effect of propofol on nitrous oxide antinociception was evaluated with tail flick latency tests. Both inhaled isoflurane and intravenous propofol inhibited nitrous-oxide-induced activation of CRF neurons, suggesting that these general anesthetics may inhibit one of the analgesic mechanisms of nitrous oxide. Indeed, propofol inhibited the antinociceptive action of nitrous oxide, as evaluated with tail flick latencies (TFL).     

Pre- and postsynaptic volatile anaesthetic actions on glycinergic transmission to spinal cord motor neurons

1. A common anaesthetic endpoint, prevention of withdrawal from a noxious stimulus, is determined primarily in spinal cord, where glycine is an important inhibitory transmitter. To define pre- and postsynaptic anaesthetic actions at glycinergic synapses, the effects of volatile anaesthetic agents on spontaneous and evoked glycinergic currents in spinal cord motor neurons from 6 - 14-day old rats was investigated. 2. The volatile anaesthetic agents enflurane, isoflurane and halothane significantly increased the frequency of glycinergic mIPSCs, enflurane to 190.4% of control+/-22.0 (mean+/-s.e.m., n=7, P<0.01), isoflurane to 199.0%+/-28.8 (n=7, P<0.05) and halothane to 198.2%+/-19.5 (n=7, P<0.01). However without TTX, isoflurane and halothane had no significant effect and enflurane decreased sIPSC frequency to 42.5% of control+/-12.4 (n=6, P<0.01). All the anaesthetics prolonged the decay time constant (tau) of both spontaneous and glycine-evoked currents without increasing amplitude. With TTX total charge transfer was increased; without TTX charge transfer was unchanged (isoflurane and halothane) or decreased (enflurane). 3. Enflurane-induced mIPSC frequency increases were not significantly affected by Cd(2+) (50 microM), thapsigargin (1 - 5 microM), or KB-R7943 (5 microM). KB-R7943 and thapsigargin together abolished the enflurane-induced increase in mIPSC frequency. 4. There are opposing facilitatory and inhibitory actions of volatile anaesthetics on glycine release dependent on calcium homeostatic mechanisms and sodium channels respectively. Under normal conditions (no TTX) the absolute amount of glycinergic inhibition does not increase. The contribution of glycinergic inhibition to anaesthesia may depend on its duration rather than its absolute magnitude.     

Brain pattern of histone H3 phosphorylation after acute amphetamine administration: its relationship to brain c-fos induction is strongly dependent on the particular brain area

Recent evidence strongly suggests a critical role of chromatin remodelling in the acute and chronic effects of addictive drugs. We reasoned that Immunohistochemical detection of certain histone modifications may be a more specific tool than induction of immediate early genes (i.e. c-fos) to detect brain areas and neurons that are critical for the action of addictive drugs. Thus, in the present work we studied in adult male rats the effects of a high dose of amphetamine on brain pattern of histone H3 phosphorylation in serine 10 (pH3S(10)) and c-fos expression. We firstly observed that amphetamine-induced an increase in the number of pH3S(10) positive neurons in a restricted number of brain areas, with maximum levels at 30 min after the drug administration that declined at 90 min in most areas. In a second experiment we studied colocalization of pH3S(10) immunoreactivity (pH3S(10)-IR) and c-fos expression. Amphetamine increased c-fos expression in medial prefrontal cortex (mPFC), dorsal striatum, nucleus accumbens (Acb), major Island of Calleja (ICjM), central amygdala (CeA), bed nucleus of stria terminalis lateral dorsal (BSTld) and paraventricular nucleus of the hypothalamus (PVN). Whereas no evidence for increase in pH3S(10) positive neurons was found in the mPFC and the PVN, in the striatum and the Acb basically all pH3S(10) positive neurons showed colocalization with c-fos. In ICjM, CeA and BSTld a notable degree of colocalization was found, but an important number of neurons expressing c-fos were negative for pH3S(10). The present results give support to the hypothesis that amphetamine-induced pH3S(10)-IR showed a more restricted pattern than brain c-fos induction, being this difference strongly dependent on the particular brain area studied. It is likely that those nuclei and neurons showing pH3S(10)-IR are more specifically associated to important effects of the drug, including neural plasticity. This article is part of a Special Issue entitled 'Post-Traumatic Stress Disorder'.     

帕罗西汀对心理应激大鼠下丘脑室旁核c-fos表达的影响

目的:观察帕罗西汀对心理应激大鼠下丘脑c fos表达的影响,以揭示帕罗西汀治疗心理应激引起焦虑的分子作用机制。方法:建立大鼠心理应激模型,观察抗焦虑药物帕罗西汀用药组大鼠血浆皮质醇和下丘脑c fos的表达。结果:与正常对照组比较,各应激组大鼠血浆皮质醇含量明显升高,下丘脑室旁核c fos表达显著增加,而帕罗西汀单次、连续给药能减少应激大鼠血浆皮质醇含量和下丘脑室旁核c fos表达。结论:帕罗西汀通过抑制c fos基因表达,下调下丘脑垂体肾上腺轴(HPA轴)水平,从而发挥中枢应激调节作用。     

Respiratory and cardiovascular effects of halothane, isoflurane and enflurane delivered via a Jackson-Rees breathing system in temperature controlled and uncontrolled rats

We studied the respiratory and cardiovascular effects of 1.25 MAC halothane, isoflurane and enflurane in oxygen delivered via the Jackson-Rees breathing system in 10 rats. Mean arterial pressure, heart rate and respiratory rate were depressed significantly (P less than 0.05) in rats (n = 5) whose body temperature was not controlled after 2 hr of anesthesia regardless of the inhalational agent. Respiratory and metabolic acidosis developed. The respiratory and cardiovascular depression was most marked under enflurane anesthesia. In normothermic rats (n = 5) the initial cardiovascular depression stabilized after 30 min of halothane and isoflurane anesthesia. Moderate respiratory depression developed (PCO2 48.42 +/- 2.48 torr with halothane vs. 41.02 +/- 1.68 torr with isoflurane). Because the cardiovascular and respiratory changes caused by halothane and isoflurane were far less than changes produced by enflurane, halothane or isoflurane is preferable to enflurane for maintaining anesthesia in rats. Maintenance of constant temperature minimizes the cardiovascular and respiratory disturbances.     

不同间歇低氧方式对内皮细胞c-fos mRNA表达水平的影响

【摘要】目的 测定不同程度、频率间歇低氧（IH）条件下,人脐静脉内皮细胞即刻早期基因c-fos mRNA的表达水平。方法在自制细胞培养舱中程控产生预制的IH/ROX（再氧和）暴露环境,将内皮细胞暴露于该环境共60次循环,分为A、B、C组,每组包括5个小组。A组分正常氧组、标准孵箱对照组、持续低氧（CH）组、1.5%O2 IH组、10%O2 IH组。B、C组分别为1.5%O2,10%O2的不同IH频率组,低氧时间均为15s,循环次数均为60次,ROX时间不同,总循环时间不同,分别为1.5h组、3h组、5h组、6.5h组、9.5h共5个小组。采用Real-time PCR方法测定c-fos mRNA的表达水平。结果正常氧组与CH组的c-fos mRNA表达水平差异无统计学意义。1.5%O2 IH组、10%O2 IH组c-fos mRNA表达水平均高于正常氧组,且1.5%O2 IH组高于10%O2 IH组（P<0.01）。IH程度相同,随着ROX时间延长,c-fos mRNA表达水平均呈现先逐渐增加,后逐渐下降的规律,5h组c-fos mRNA表达水平明显高于其余各组（P<0.01）。结论 IH/ROX暴露可诱导内皮细胞即刻早期基因c-fos mRNA表达,这一过程与IH程度及频率密切相关。      

大鼠脑二次损伤凋亡相关基因的表达

目的 探讨大鼠脑二次损伤(SBI)c-fos、bcl-2、bcl-xL基因表达和细胞凋亡关系.方法 40只大鼠随机分为正常对照组10只、脑缺血组10只、颅脑损伤组10只和SBI组10只,以免疫组织化学方法,检测脑神经细胞中c-foe、bcl-2、bcl-xL的表达水平;以原位细胞凋亡(TUNEL)法检测神经细胞凋亡水平.结果 颅脑损伤组、SBI组皮层区c-fos基因表达(23.6±9.4)、(37.1±5.5)阳性细胞数/个/H均明显高于脑缺血组(5.6±1.4)阳性细胞数/个/H(t=3.458,t=3.648,均P<0.01);颅脑损伤组、SBI组皮层区bcl-2基因表达(18.2±4.6)、(15.6±3.7)阳性细胞数/个/H低于脑缺血组(23.6±4.3)阳性细胞数/个/H(t=2.345,t=2.447,均P<0.05);脑缺血组、颅脑损伤组和SBI组bcl-xL基因表达变化不大;SBI组皮层区细胞凋亡(36.6±5.3)个细胞/0.1mm2高于颅脑损伤组(21.6±4.4)个细胞/0.1mm2(t=2.378,P<0.05);细胞凋亡水平与bcl-2表达均呈负相关(r=-0.857,P<0.01).结论 脑二次损伤c-fos、bcl-2、bcl-xL基因表达增加并与神经细胞凋亡水平密切相关.     

脑缺血再灌注损伤大鼠海马神经元凋亡及c—fos蛋白表达研究

目的：观察脑缺血再灌注损伤大鼠海马神经元凋亡及c-fos蛋白的表达。方法：采用大脑中动脉阻断法制备大鼠脑缺血再灌注模型,取海马组织,用免疫组织化学方法检测海马神经元c-fos蛋白表达及TUNEL法观察细胞凋亡情况。结果：脑缺血再灌注损伤大鼠与对照组比较海马区c-fos蛋白阳性细胞表达增强（P〈0．05）,凋亡细胞表达增多（P〈0．05）。结论：脑缺血再灌注损伤大鼠海马区c-fos蛋白阳性细胞表达增强,凋亡细胞表达增多。     

硒化壳聚糖对HL60细胞的诱导分化作用

目的:研究硒化壳聚糖对人早幼粒细胞性白血病HL60细胞分化的影响,并探讨该影响与细胞c-myc和c-fos蛋白表达的关系。方法:取HL60细胞分为5组,分别为25、50、100mg·L-1硒化壳聚糖组、空白对照组(培养液)和阳性对照组(二甲基亚砜)。各组经相应试药作用后,采用硝基蓝四氮唑(NBT)还原法检测HL60细胞分化情况,观察NBT阳性细胞数;流式细胞术检测c-myc和c-fos蛋白表达。结果:与空白对照组比较,硒化壳聚糖各组作用与阳性对照组相似,NBT还原阳性细胞明显增多,c-myc蛋白表达显著下降(P<0.01或P<0.05),c-fos蛋白表达显著升高(P<0.01或P<0.05)。结论:硒化壳聚糖可能通过增强HL60细胞c-fos表达及下调c-myc表达来诱导细胞分化。