异氟醚、安氟醚麻醉诱导期大鼠边缘系统部分核团一氧化氮合酶阳性神经元的改变

目的 观察异氟醚、安氟醚诱导麻醉对大鼠边缘系统部分核团一氧化氮合酶(NOS)阳性神经元的的改变,探讨异氟醚、安氟醚麻醉诱导期的作用机制。方法 18只SD雄性大鼠随机分为3组:对照组、安氟醚组、异氟醚组。对照组动物除不吸入麻醉气体外,其他条件均与两麻醉组相同。安氟醚组、异氟醚组大鼠分别吸入2％安氟醚或2％异氟醚至步态不稳、一侧肢体着地,即翻正反射即将消失时,移出麻醉箱,立即取标本。用NADPH-d组化法观察吸入2％异氟醚、2％安氟醚诱导麻醉对大鼠边缘系统部分核团NOS阳性神经元数量和灰度值的影响。结果 安氟醚组大鼠脑的外侧隔核、下丘脑室旁核、下丘脑室周核、视上核、杏仁基外侧核和伏隔核等6个核团NOS阳性神经元数量和染色深度均低于对照组,异氟醚组在上述6个核团中NOS阳性神经元的数量和平均灰度水平也低于对照组,下丘脑室周核和视上核NOS阳性神经元数目有减少趋势,但与对照组比较差异无统计学意义(P>0.05),其余核团与对照组比较差别均有显著性(P<0.01)。结论 异氟醚、安氟醚诱导期的作用机理可能与边缘系统部分核团NOS阳性神经元的改变有关。     

异氟醚对心血管的影响

新的吸入麻醉药——异氟醚的应用,使吸入麻醉进入了一个新的阶段。异氟醚为安氟醚的同分异构体,其物理性状和药理作用与安氟醚相同,但在药代动力学方面,其在体内蓄积量少,毒性低;在药效动力学方面,其麻醉效能强。与同类吸入麻醉药相比,异氟醚具育独特的心血管效应。本文将从心肌收缩力、心脏前负荷、后负荷以及心律等方面分别讨论异氟醚对心血管的影响。     

吸入异氟醚或地氟醚预处理对心内直视手术小儿围术期心肌的保护作用

吸入性麻醉药具有与缺血预适应相仿的效应,使心肌梗死范围减小,产生直接的心脏保护作用,这种现象称之为“吸入性麻醉药预处理”。异氟醚和地氟醚是卤族氟类吸入麻醉药,在临床麻醉上广泛使用,特别是用于小儿的麻醉诱导和维持。但异氟醚或地氟醚预处理对小儿围术期心肌的保护作用尚未定论,本研究拟观察吸入异氟醚或地氟醚预处理对体外循环(CPB)下心内直视手术小儿围术期心肌的保护作用。     

深低温对吸入麻醉药的MAC,心脏麻醉指数和心肌稳定性的影响

目的:研究深低温对吸入麻醉药MAC、心脏麻醉指数和心肌稳定性的影响。方法:新西兰白兔40只,随机分为氟烷、安氟醚、异氟醚和七氟醚组。采用夹尾试验法测定常温下(38℃±0.5℃)的最低肺泡有效浓度(MAC)。行体表降温后测定深低温下(23℃±0.5 ℃)的MAC。维持深低温增加吸入性麻醉药的浓度,同时用50Hz、25V电压胸外电击心脏。记录出现室颤或室性心律失常时的肺泡呼气末吸入麻醉药浓度。结果:从38℃到23℃兔体温每降低1℃,MAC下降值为:氟烷5.1％、安氟醚3.6％、异氟醚4.4％、七氟醚4.3％;氟烷、安氟醚、异氟醚和七氟醚心脏麻醉指数分别为4.4、3.18、6.25和4.6,异氟醚明显高于其它麻醉药;麻醉药浓度8MAC以内安氟醚和氟烷发生室颤的机率(100％)明显高于七氟醚和异氟醚(40％)。结论:异氟醚是深低温麻醉的最佳选择用药,而安氟醚则不宜用于低温麻醉。     

吸入麻醉药对兔肾交感神经活动的影响

目的比较吸入麻醉药对交感神经活动和血液动力学的影响。方法18只兔被随机分为三组:安氟醚组、异氟醚组和地氟醚组。兔麻醉、肌松和人工通气后,暴露肾交感神经并记录其电生理活动。分别吸入呼气末浓度为0.8%、1.6%、2.4%、3.2%安氟醚,0.6%、1.2%、1.8%、2.4%异氟醚,或3.0%、6.0%、9.0%、12.0%地氟醚。结果交感神经活动在兔吸入2.4%安氟醚、0.6%异氟醚和6.0%地氟醚时分别增加到44%、36%和32%,当进一步增加吸入麻醉药的浓度则抑制肾交感神经活动。血压随着吸入麻醉药浓度的增加不断下降而心率除了2.4%异氟醚诱发心率减慢外无明显变化。结论安氟醚、异氟醚和地氟醚具有双向作用,低浓度兴奋交感神经,高浓度抑制交感神经活动和降低血压。     

婴幼儿腹部手术两种麻醉方法比较

目的:观察婴幼儿常用的两种麻醉方法氯胺酮复合硬膜外麻醉和氯胺酮复合安(异)氟醚吸入麻醉的优缺点。方法:将78例病人随机分为氯胺酮复合硬膜外组、氯胺酮复合安(异)氟醚组,分别在围麻醉期对其生命体征、麻醉诱导时间及清醒时间、麻醉药物用量等方面观察。结果:氯胺酮复合硬膜外组麻醉诱导时间20±3min、氯胺酮平均用量16mg/kg、术中比术前血压下降10±5mmHg、术后清醒时间5±3/min、术中复用安定4例;氯胺酮复合安(异)氟醚吸入组麻醉诱导时间7±2min、氯胺酮平均用量13.6mmHg、术中比术前血压下降3±1mmHg、术后清醒时间1±1min、术中复用安定0例。结论:氯胺酮复合安(异)氯醚吸入组在麻醉诱导时间、氯胺酮用量、术后清醒时间、对循环系的干扰方面明显优于氯胺酮复合硬膜外组。     

腹部手术患者吸入七氟醚与异氟醚麻醉恢复的比较

目的比较腹部手术患者吸入七氟醚与异氟醚麻醉恢复的情况。方法全麻下行开腹手术患者40例,随机分为2组（n=20）：七氟醚组（S组）及异氟醚组（Ⅰ组）。麻醉诱导后行气管插管,机械通气。诱导后吸入纯氧,氧流量2 L/min,30min后调整为1 L/min。手术开始前,调整吸入麻醉药的呼气末浓度为1.0 MAC。麻醉维持：吸入七氟醚或异氟醚,间断静脉注射罗库溴铵和芬太尼,维持血压和心率波动幅度不超过基础值30%。缝皮结束时,停止吸入七氟醚或异氟醚,纯氧流量调整为5 L/min。记录睁眼时间（停止吸入麻醉药到睁眼的时间）、拔除气管导管时间（停止吸入麻醉药到拔除气管导管的时间）、Aldrete评分达到9分时间（从停止吸入麻醉药计时）及麻醉后恢复室（PACU）停留时间。记录吸入麻醉药用量。结果与Ⅰ组比较,S组睁眼时间、拔除气管导管时间、Aldrete评分达到9分时间及PACU停留时间缩短（P〈0.05）,吸入麻醉药的总用量和单位时间用量差异无统计学意义（P〉0.05）。结论与异氟醚比较,吸入七氟醚患者麻醉恢复较快,且麻醉恢复质量较好。     

静吸复合麻醉下七氟醚与异氟醚对颅内压的影响

目的:在颅内顺应性正常神经外科病人,观察1.0 MAC七氟醚与异氟醚对颅内压的影响。方法:垂体瘤或颅咽管瘤手术病人16例,随机分为两组:A组为咪唑安定 芬太尼 1.0 MAC异氟醚;B组为咪唑安定 芬太尼 1.0 MAC七氟醚。选择L_(3～4)行蛛网膜下腔穿刺。麻醉诱导采用芬太尼-咪唑安定-阿曲库铵。插管后维持稳定30分开始吸入七氟醚(或异氟醚)。分别于麻醉前、吸入麻醉药前、达预定呼气末浓度30分内观察监测指标。结果:1.0 MAC七氟醚和异氟醚均可显著降低脑灌注压,异氟醚作用较强。吸入1.0 MAC七氟醚后颅内压首先呈显著性下降,15分后回复至基础水平。吸入1.0 MAC异氟醚后颅内压无显著性变化。结论:在颅内顺应性正常患者,1.0 MAC七氟醚和异氟醚均可安全用于神经外科麻醉。     

安氟醚、异氟醚、氟烷和甲氧氟烷在间脑的作用部位研究

应用FOS蛋白免疫组织化学方法研究临床上常用的四种吸入麻醉药在间脑的作用部位,为进一步探讨吸入麻醉机理提供形态学定位依据。材料和方法成年SD大鼠30只均分为对照组、2％安氟醚、2％异氟醚、2％氟烷和2％甲氧氟烷五组。对照组除不吸入麻醉气体外,其它条件均与麻醉组相同,1小时后用戊巴比妥钠麻醉后立即开胸经升主动脉灌注4％多聚甲醛。麻醉组吸入不同麻醉药后1小时开胸灌注固定90分,取全脑置于20％庶糖液中过夜,连     

安氟醚麻醉诱导Fos蛋白与脑啡肽在大鼠中枢神经系统的表达及定位研究

目的观察安氟醚麻醉后大鼠中枢神经系统各部位Fos蛋白与脑啡肽(ENK)的表达及共存情况.方法成年SD大鼠(第四军医大学实验动物中心提供)12只,雌雄不拘,体重195～223g,随机分为对照组和实验组,每组6只.实验组吸入2%安氟醚2h,对照组不吸入麻醉药,其余条件同实验组.经左心室灌注生理盐水100ml洗去全身血液,继之灌注含4%多聚甲醛的0.1mol/LPB500ml,固定90min,取全脑和脊髓冰冻连续冠状切片,双标记免疫组化染色,低倍光镜下观察染色阳性细胞的分布情况;高倍镜下观察鉴别Fos染色免疫阳性(FLI)细胞,ENK染色免疫阳性(ELI)细胞以及Fos、ENK共同表达(FLI/ELI)细胞,计数神经核团一个高倍视野内的阳性细胞数目.结果对照组中,ELI神经元较多,FLI神经元少量、散在无规律地分布,FLI/ELI神经元极少见.实验组中可明显观察到ELI、FLI、FLI/ELI三种神经元,主要分布在大脑额顶皮质、外侧隔核、杏仁核、海马CA1区、丘脑室旁核、丘脑腹外侧核、僵核、下丘脑腹内侧核、视上核、网状结构、脚间核、中脑中央灰质及脊髓背角等神经核团,这些核团内FLI和ELI神经元数量与对照组比较显著增多(P＜0.05),在其它核团内无显著变化;Fos、ENK双标神经元约占FLI神经元的15%～42%.结论安氟醚可诱导Fos蛋白在某些神经核团内表达并使其内ENK增多;Fos蛋白可能作为脑啡肽基因的转录调控因子,引起ENK的变化.     

七氟醚麻醉对新生大鼠杏仁核DNA甲基转移酶mRNA表达的影响

目的 探讨七氟醚麻醉对新生大鼠杏仁核DNA甲基转移酶(DNMT)mRNA表达的影响.方法 新生(出生8 d)SD大鼠42只,采用随机数字表法,将其随机分为2组(n=21),对照组:不给予任何处理;实验组:吸入5%七氟醚1 min后,吸入浓度调整为3%维持4 h.实验组分别于停止吸入即刻及停止吸入后24 h时,处死大鼠,取杏仁核,测定DNMT1 mRNA、DNMT3a mRNA、DNMT3b mRNA的表达;停止吸入即刻取动脉血样,进行血气分析.对照组于相应时间点进行处理.结果 与对照组比较,实验组DNMT1 mRNA、DNMT3a mRNA表达均下调(P＜0.05),DNMT3b mRNA表达和血气分析指标差异无统计学意义(P＞0.05).结论 七氟醚麻醉可下调新生大鼠杏仁核DNMT1 raRNA和DNMT3a mRNA的表达,该作用可能会导致发育期中枢神经功能损伤.

Abstract：

Objective To investigate the effect of sevoflurane anesthesia on DNA methyltransferase (DNMT) mRNA expression in neonatal rat amygdala. Methods Forty-two 8-day-old SD rats were randomly divided into 2 groups ( n = 21 each): control group and experimental group. 5% sevoflurane was inhaled for 1 min, and then the inhaled concentration of sevoflurane was decreased to 3 % and maintained for 4 h. The rats were sacrificed at the end of sevoflurane inhalation and 24 h after the end of sevoflurane inhalation, and amygdala was removed for determination of DNMT, mRNA, DNMT3, mRNA and DNMT3b mRNA expression by RT-PCR. Blood samples were taken at the end of sevoflurane inhalation for blood gas analysis. Results Compared with control group, the DNMT, mRNA and DNMT3, mRNA expression was down-regulated (P ＜ 0.05). There were no significant differences in DNMT3b mRNA expression and parameters of blood gas analysis between the two groups (P ＞ 0.05). Conclusion Sevoflurane anesthesia can down-regulate DNMT, mRNA and DNMT,, mRNA expression in neonatal rat amygdala, which may result in functional deficits during the development of central nervous system.     

Increased synthesis of nitric oxide in rat brain cortex due to halogenated volatile anesthetics confirmed by EPR spectroscopy

BACKGROUND: Halogenated volatile anesthetics (HVAs) are considered to be inhibitors of nitric oxide synthase (NOS). On other hand, NO mediates the vasodilation produced by HVAs. Thus, both increase and decrease of NO concentration in brain tissues are possible during anesthesia. Previously, we have observed an increase of NO content in rat brain cortex under halothane anesthesia. The goal of this study was to determine whether the observed phenomenon was general for this anesthetic group, if it was specific for brain cortex, and if the NO increase was due changes in NOS activity. METHODS: NO scavengers were injected to adult rats 30 min prior to anesthesia. Rats were anesthetized by inhalation of an O2 mixture with volatile anesthetics (1.5% for halothane; 1% for isoflurane, 2% for sevoflurane). After 30 min of anesthesia, rats were decapitated and brain cortex, cerebellum, liver, heart, kidneys and testes were dissected, frozen in liquid nitrogen and subjected to EPR spectroscopy. Nitric oxide content was determined quantitatively based on the intensity of the NO-Fe-DETC complex spectrum and its comparison with the calibration curve. RESULTS: In rats anesthetized with HVAs, we observed a greater than twofold increase of NO content in brain cortex as compared to the nonanesthetized animals. No significant changes were detected in other organs. The NOS inhibitor N(omega)-nitro-L-arginine abolished the increase of NO content in brain produced by volatile anesthetics. CONCLUSION: The action of volatile anesthetics is coupled with an increase of NO content in the cortex dependent on NOS activity.     

癌基因产物c-jun和c-fos在髓母细胞瘤中的表达及临床意义

目的　了解c jun和c fos在髓母细胞瘤中的表达情况及其与预后的关系。方法　通过免疫组化方法测定c jun和c fos蛋白在 70例髓母细胞瘤和 10例正常小脑组织中的表达情况 ,并结合临床资料 ,对病人生存时间与c jun和c fos表达阳性率之间的关系进行分析。 结果　 (1)正常小脑组织标本不表达c jun和c fos;而髓母细胞瘤中多为不同程度的阳性表达 ,且以高阳性率为主 ,并发现阳性染色主要位于肿瘤细胞核 ,部分胞浆也有染色。 (2 )c jun和c fos表达呈正相关 (r =0 4 93,P <0 0 1) ;二者协同性较强。 (3)生存时间与c jun、c fos表达阳性率呈负相关 (c jun :r =- 0 4 4 7,P <0 0 1;c fos:r =- 0 5 90 ,P <0 0 1) ;c jun、c fos表达强度愈高 ,病人的生存率就愈低 ,生存时间就越短。结论　c jun和c fos在髓母细胞瘤组织中呈高表达。c jun和c fos二者在髓母细胞瘤中表达具有协同性。c jun、c fos在肿瘤中的阳性表达率与髓母细胞瘤病人的预后呈显著负相关     

甲氧氟烷吸入麻醉诱导中枢神经系统c-fos基因的表达

目的：了解甲氧氟烷吸入麻醉在中枢神经系统的作用部位。方法：应用免疫组织化学方法,光镜观察Ｆｏｓ蛋白阳性神经元在中枢神经系统的分布并计数。结果：大鼠吸入甲氧氟烷浓度为０．７５－１．５％和２．０％麻醉１小时后,Ｆｏｓ阳性神经元主要分布于可仁核族、弓状核、丘脑腹前核（ＡＶ）、终纹床核（ＢＳＴ）、中央灰质（ＰＡＯ）、 内侧梨状核、下丘脑背内侧核、Ｅ－Ｗ核（ＥＷ）、脚间核（ＩＰ）、内外侧僵核（Ｈｂ）、外侧隔     

Effect sites of anesthetics in the central nervous system network--looking into the mechanisms for natural sleep and anesthesia

We showed the effect sites of anesthetics in the central nervous system (CNS) network. The thalamus is a key factor for loss of consciousness during natural sleep and anesthesia. Although the linkages among neurons within the CNS network in natural sleep are complicated, but sophisticated, the sleep mechanism has been gradually unraveled. Anesthesia disrupts the link-ages between cortical and thalamic neurons and among the cortical neurons, and thus it loses the integration of information derived from the arousal and sleep nuclei. It has been considered that anesthesia does not share the common pathway as natural sleep at the level of unconsciousness, because anesthetics have multiple effect sites within CNS network and may induce disintegration among neurons. Recent literatures have shown that the effects of anesthetics are specific rather than global in the brain. It is interesting to note that thalamic injection of anti-potassium channel materials restored consciousness during inhalation anesthesia, and that the sedative components of certain intravenous anesthesia may share the same pathway as natural sleep. To explore the sensitivity and susceptibility loci for anesthetics in the thalamocortical neurons as well as arousal and sleep nuclei within CNS network may be an important task for future study.     

Lignocaine–induced convulsion does not induce c–fos protein (c–Fos) in rat hippocampus

Recent studies have shown that proto–oncogene c–fos mRNA is induced in the central nervous system by a variety of stimuli including generalised convulsions. In this study, the expression of c–fos protein (c–Fos) following lignocaine–induced convulsions was examined and compared with that following convulsions induced by non–anesthetic convulsants, such as pentylenetetrazol, kainic acid and electroconvulsive shocks, in rat brain.
Administration of 120 mg kg^-1 lignocaine by the intraperitoneal route induced generalised convulsions in all rats examined within 10 min. C–Fos was markedly induced in the piriform cortex and amygdala, and slightly induced in the neocortex and thalamus, while no c–Fos expression was observed in the hippocampus. In contrast, c–Fos expression following generalised convulsions induced by non–anaesthetic convulsants was very marked in the hippocampal region, piriform cortex and amygdala, and extended to the thalamus and neocortex.
These results contradict those of previously reported local cerebral metabolic studies using 2–deoxyglucose as a metabolic marker, and suggest that lignocaine–induced convulsions, unlike those induced by non–anaesthetic convulsants, may not cause severe sequelae (plastic changes) in the hippocampus.     

异氟醚麻醉下人身体感觉诱发电位的改变

目的：探讨脊髓是异氟醚的重要作用部位,方法：对18例妇科手术患者行异氟醚麻醉,并以硬膜外阻滞作对照,刺激踝部胫神经,监测并记录头颈部体感诱发电位,记录分3个阶段：基础值,异氟醚麻醉,硬膜外腔阻滞,结果：异氟醚麻醉,硬膜外腔阻滞均可使下肢体感诱发电位的潜伏期明显延迟,结论：异氟醚麻醉对脊髓具有明显的抑制作用,脊髓可能是异氟醚麻醉作用的重要中枢部位。     

酪氨酸激酶途径在成骨细胞增殖及c-fos表达中的作用

目的探讨酪氨酸激酶信息传递途径在成骨细胞增殖及ｃ－ｆｏｓ表达中的作用。方法采用阶段性酶消化法分离拳头新生大鼠颅盖骨居骨细胞,用ＭＴＴ法观察成骨细胞增殖,用免疫组化ＳＰ法结合计算机图像处理系统检测成骨细胞ｃ－ｆｏｓ表达。结果酪氨酸激酶抑制剂Ｇｅｎｉｓｔｅｉｎ和ＨｅｒｂｉｍｙｃｉｎＡ抑制成骨细胞增殖,且两者均部分阻断血清刺激的成骨细胞ｃ－ｆｏｓ表达。结论血清刺激和维持成骨细胞增殖及诱导ｃ－ｆｏｓ表达均     

体外刺激对培养成纤维细胞功能与表达c—fos基因的影响

目的 研究采用碱性成纤维细胞生长因子（bFGF)刺激对体外培养成纤维细胞形态、功能以及表达原癌基因c-fos的影响,探讨成纤维细胞生长因子与原癌基因之间在调控创面愈合中可能的网络机制。方法 将处于对数生长期的乳鼠成纤维细胞分成bFGF刺激组织和对照组,在分别采用bFGF和对照物刺激后继续培养,于刺激后1小时和3、5及7天采集细胞用于形态学和细胞活力检测。同时用SP法对原位培养法和甩片法收集的成纤维细胞检测c-fos基因表达。结果 培养的成纤维细胞经bFGF刺激后其形态较对照明显增大,MTT检测活性明显增设,在刺激后表达c-fos基因显著增加,其中以刺激后1小时最为明显。结论 bFGF刺激可以使培养的成纤维细胞形态与功能发生明显改变,使c-fos基因表达显著增加。结合既往研究表明,c-fos不仅可以直接上调bFGF基因表达,同时bFGF本身也可以诱导c-fos基因表达,表明二者之间可能存在相互作用的网络机制。其可能的调控途径涉及ras以及酪氨酸激酶等。