异氟醚对福尔马林刺激诱发间脑FoS蛋白的影响

异氟醚是临床上广泛应用的一种吸入麻醉药,它具有诱导快、苏醒快、对循环干扰小、副作用少等优点,它单用或复合其他麻醉药可抑制伤害性刺激引起的运动反应。本实验通过观察异氟醚对伤害性刺激诱发中枢神经系统中c-fos表达的影响来探讨其可能作用的部位和作用机制。     

心脏大血管手术麻醉的进展

一、麻醉方面 大量前瞻性研究集中观察选择哪一类麻醉药影响心脏手术后的效果。Tuman等认为麻醉药选择对冠心病或心脏瓣膜手术后效果几乎没有影响。以芬太尼、苏芬太尼、安定和氯胺酮以及氟烷为主要药物,或以安氟醚、异氟醚等为辅助药物等,均无明显差异。即使认为异氟醚有冠状血管扩张作用,但未发现有不良影响。有研究认为异氟醚对有窃血倾向解剖的病人,其心肌缺血发生率并未比其他麻醉药高。有报道360例心脏瓣膜     

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。     

吸入麻醉药对心肌收缩力的抑制作用

常用的吸入麻醉药,如氟烷、安氟醚、异氟醚与七氟醚等,在产生全麻作用的同时,也降低了心肌的收缩力。导致这种负性肌力作用的因素有很多。近年来,对其作用机制的研究越来越深入,提出了一些新的观点,现就此予以综述。     

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。     

异氟醚预处理在脑缺血半暗带保护中的作用机制研究进展

背景 缺血半暗带为脑缺血疾病临床治疗中的主要靶点,然而有效安全的非溶栓防治措施多年来一直未有突破.近年来有研究发现吸入麻醉药异氟醚预处理对脑缺血半暗带有保护作用,为脑缺血的防治提供了新的思路.目的 分析总结异氟醚预处理在脑缺血半暗带保护中的作用及其可能的机制.内容 首先介绍缺血半暗带在脑缺血疾病中的地位及复杂性；然后描述异氟醚预处理对脑缺血半暗带保护作用的现状并分析其可能参与的机制. 趋向 Toll样受体4信号通路的参与及其他保护机制还有待进一步探索,为其临床应用奠定更有力的证据,同时还有利于从机制中挖掘治疗脑缺血疾病的新方向.     

在心脏手术中异氟醚的应用

异氟醚是二次大战以后最近问世的氟化吸入麻醉药。经动物和临床验证结果提示它比其他药物为好。在需要保护心肌和心排出量(CO)的心脏手术病人中,应用低浓度异氟醚有特殊的优点。一、异氟醚的心血管效应1.心肌状态(myocardial performance):它的浓度一旦超过2％,则导致与剂量相关的极为严重的抑制,这种效应方式与氟烷、安氟醚等吸入麻醉相似。它对心肌收缩力的抑制可能是通过降低CGMP的水平和/或降低收缩蛋白的钙活性。与氟烷或安氟醚不同之     

吸入麻醉药的心肌缺血预处理效应

缺血预处理是机体对短暂缺血损害的一种主动、适应性反应，能增强组织对缺血的耐受性，尤其对心肌再灌注损伤有保护作用，是近年来保护脏器的一种新概念。吸入麻醉药，如异氟醚、七氟醚等可产生类似于缺血预处理的效应，提供有效的脏器保护作用，其机制与KATP通道、腺苷释放和蛋白激酶有关。迄今，吸入麻醉药预处理已在动物实验研究方面取得了许多资料和经验。临床应用的零星研究报道结果虽令人鼓舞，但尚需进一步研究。     

乳化异氟醚预处理对兔心肌缺血再灌注损伤的影响

挥发性麻醉药异氟醚亦可以静脉方式给药,为异氟醚应用提供便利的给药方式,并可产生良好的麻醉作用[1].吸入异氟醚预处理可减轻心肌缺血再灌注损伤[2,3],而静脉注射异氟醚预处理能否发挥器官保护作用有待进一步探讨.     

Was wissen wir über Narkosemechanismen?

Despite the increase of molecular knowledge in anesthesia research over the past decades there is still ongoing discussion about the mechanisms of anesthesia. This article focuses on presenting anesthetic sensitive ligand and voltage gated ion channels. The impact on anesthetic modulated ion channels is summarized for clinically commonly used anesthetics isoflurane, propofol and ketamine. Furthermore, the anesthetic features hypnosis, unresponsiveness to surgical incision and amnesia and their putative relevant anatomical sites in the central nervous system are briefly introduced.     

Mutation of alpha1G T-type calcium channels in mice does not change anesthetic requirements for loss of the righting reflex and minimum alveolar concentration but delays the onset of anesthetic induction

BACKGROUND: T-type calcium channels regulate neuronal membrane excitability and participate in a number of physiologic and pathologic processes in the central nervous system, including sleep and epileptic activity. Volatile anesthetics inhibit native and recombinant T-type calcium channels at concentrations comparable to those required to produce anesthesia. To determine whether T-type calcium channels are involved in the mechanisms of anesthetic action, the authors examined the effects of general anesthetics in mutant mice lacking alpha1G T-type calcium channels. METHODS: The hypnotic effects of volatile and intravenous anesthetics administered to mutant and C57BL/6 control mice were evaluated using the behavioral endpoint of loss of righting reflex. To investigate the immobilizing effects of volatile anesthetics in mice, the minimum alveolar concentration (MAC) values were determined using the tail-clamp method. RESULTS: The 50% effective concentration for loss of righting reflex and MAC values for volatile anesthetics were not altered after alpha1G channel knockout. However, mutant mice required significantly more time to develop anesthesia/hypnosis after exposure to isoflurane, halothane, and sevoflurane and after intraperitoneal administration of pentobarbital. CONCLUSIONS: The 50% effective concentration for loss of righting reflex and MAC values for the volatile anesthetics were not altered after alpha1G calcium channel knockout, indicating that normal functioning of alpha1G calcium channels is not required for the maintenance of anesthetic hypnosis and immobility. However, the timely induction of anesthesia/hypnosis by volatile anesthetic agents and some intravenous anesthetic agents may require the normal functioning of these channel subunits.     

Electrophysiological approach to mechanisms for actions of general anesthetics

Although general anesthetics were first used more than 160 years ago, their mechanisms have remained mysterious. During the past decade, significant progress in our understanding of general anesthetic action at the cellular and network system levels has been made. Our recent work demonstrates (a) that intravenous anesthetics, but not volatile agents, enhance the discharge of GABA from presynaptic terminals, (b) that intravenous anesthetics produce frequency-dependent modification (FDM) of anesthesia, and (c) that FDM is responsible for the unsuccessful immobilization or hypnosis during intravenous anesthesia. In addition, we review the development of hypothesis for anesthetic action, non-specific versus specific action, cutoff phenomenon in n-alcohols, and anesthesiological approach to consciousness.     

Mechanism of anesthesia: view from the EEG during anesthesia

It is widely known that electroencephalogram (EEG) shows dramatic changes with increase of the concentration of anesthetic. It is considered that volatile anesthetics (i. e. isoflurane, sevoflurane), barbiturates, propofol show anesthetic effect by potentiating GABAA receptor. Changing patterns of EEG by these anesthetics are quite similar. In light anesthetic level, high frequency with low amplitude waves are dominant. With increase of anesthetic concentration, waves in alpha range (8-13 Hz) become dominant. In deeper levels, powers in alpha range then become smaller and theta or delta powers become dominant. With further deeper levels, EEG waveform changes into specific pattern so-called "burst and suppression", and finally it becomes flat. The author considers that prominent alpha power indicates adequate anesthetic level. However this is not always the required condition for adequate anesthesia, because alpha power never becomes larger in some patients even when the anesthetic level was judged as adequate by concentration dependent changing patterns of EEG. As EEG changes in relation to the concentration of anesthetic, it seems to be correlated with the level of consciousness. But EEG patterns during anesthesia are mainly determined by the condition of thalamic neurons, and it would merely indicate the level of hypnosis indirectly.     

Anesthetic mechanisms in the spinal cord

The essential elements of anesthesia are : hypnosis, amnesia, analgesia, immobility, and inhibition of untoward reflexes. The spinal cord is responsible for the latter three. Suppression of excitatory transmission and stimulation of inhibitory transmission are the anesthetic mechanisms in the spinal cord. Each anesthetic, however, has a unique effect on the transmission systems in the spinal cord. Some exclusively suppress excitatory transmission or stimulate inhibitory transmission, and others have a dual effect. The minimum alveolar/anesthetic concentration (MAC) is spinally mediated. Furthermore neurons in the ventral horn of spinal cord seem to be more depressed by anesthetics than neurons in the dorsal horn of the spinal cord. The ventral spinal cord also has relation to spinal cord ischemia. Investigation of the neuroprotective effect against spinal ischemia as well as the anesthetic effect in the ventral spinal cord is a very important subject of research.     

Similar recovery from bispectral index-titrated isoflurane and sevoflurane anesthesia after outpatient gynecological surgery

STUDY OBJECTIVE: To test the hypothesis that the recovery of gynecological day-case patients is equally fast after isoflurane and sevoflurane anesthesia, when administration of the inhaled agent is adjusted by monitoring the bispectral index (BIS). DESIGN: Prospective, randomized, controlled, single-blinded clinical study. SETTING: University-affiliated women's hospital. PATIENTS: 120 adult female patients, ASA physical status I or II, scheduled for ambulatory surgery under general anesthesia. INTERVENTIONS: Patients were randomized to receive either isoflurane or sevoflurane as the maintenance anesthetic. BIS values were titrated to remain between 50 and 60 during the maintenance of anesthesia by adjusting the inspired concentration of the inhaled agent. Administration of the inhaled agent was discontinued abruptly at the end of the procedure. MEASUREMENTS: The times to achieving several recovery end points were recorded. The main outcome parameter was the time to home-readiness. In the postoperative care unit, sedation was evaluated with the digit-symbol substitution test. The degree of pain and nausea was evaluated on the visual analog scale. MAIN RESULTS: There were no statistically significant differences in the times to home-readiness, or in any other parameters of early or intermediate recovery between the 2 groups. The degrees of sedation, pain, and nausea in the postoperative care unit were similar in the 2 groups. CONCLUSIONS: Isoflurane and sevoflurane are equally acceptable maintenance anesthetics in terms of the speed and quality of recovery in gynecological ambulatory surgery patients when the dose of the inhaled agent is adjusted to achieve a BIS between 50 and 60.     

全身麻醉药物对脑电信号影响的研究进展

脑电信号是脑神经细胞在大脑皮层或头皮表面的总体反映,随着脑电信号监测技术的应用和发展,麻醉过程中进行脑电信号监测可以提示麻醉药物的作用情况,因此麻醉药物对脑电信号的影响是麻醉监测的一个重要研究主题。全身麻醉药物包括静脉麻醉药物和吸入麻醉药物,这些麻醉药物通过可逆性地抑制中枢神经系统,对大脑状态产生影响,最终产生不同程度的镇静作用。在麻醉药物的使用过程中,大脑会呈现出慢频率和大振幅的特点,但不同药物的频谱却各有差异。本文根据现有文献,对不同麻醉药物作用下脑电信号的影响进行综述,为今后的基础和临床研究提供理论基础和新的思路。     

Molecular approaches to improving general anesthetics

Over the last several decades, the average age of patients has steadily increased, whereas the use of general anesthesia and deep sedation has grown largely outside the operating room environment. Currently available general anesthetics and delivery models represent limitations in addressing these trends. At the same time, research has tremendously expanded the knowledge of how general anesthetics produce their beneficial effects and also revealed evidence of previously unappreciated general anesthetic toxicities. The goal of this review is to highlight these important developments and describe translational research on new general anesthetics with the potential to improve and reshape clinical care.     

Different effects of volatile anesthetics and polyhalogenated alkanes on depolarization-evoked glutamate release in rat cortical brain slices.

Anesthetics cause a reduction in excitatory neurotransmission that may be important in the mechanisms of in vivo anesthetic action. Because glutamate is the major excitatory neurotransmitter in mammalian brain, evaluation of anesthetic effects on induced glutamate release is relevant for studying this potential mechanism of anesthetic action. In the present study, we compared the effects of anesthetics and nonanesthetics (halogenated alkanes that disobey the Meyer-Overton hypothesis) on depolarization-evoked glutamate release. Glutamate released from rat cortical brain slices after chemically induced depolarization (50 mM KCl) was measured continuously using an enzymatic fluorescence assay. The effects of the volatile anesthetics isoflurane and enflurane were compared with the effects of the transitional compound 1,1,2-trichlorotrifluoroethane, the nonanesthetic compound 1,2-dichlorohexafluorocyclobutane, and other polyhalogenated alkanes. Tested concentrations included effective anesthetic concentrations for the anesthetics and transitional compounds, and concentrations predicted to be anesthetic based on lipid solubility for the nonanesthetics. Isoflurane dose-dependently reduced depolarization-evoked glutamate release in cortical brain slices. Isoflurane and enflurane at concentrations equivalent to 1 minimum alveolar anesthetic concentration (MAC) reduced the KCl-evoked release to 20% and 17% of control, respectively. The transitional compound 1,1,2-trichlorotrifluoroethane at 210 microM (approximately 1.2 MAC) reduced glutamate release to 47%, and the nonanesthetic 1,2-dichlorohexafluorocyclobutane increased glutamate release at 70 microM (approximately 3 MAC). These findings support the hypothesis that the modulation of excitatory neurotransmission might be responsible, in part, for in vivo anesthetic action. IMPLICATIONS: The volatile anesthetics isoflurane and enflurane reduce depolarization-evoked glutamate release in rat brain slices. The transitional compound 1,1,2-trichlorotrifluoroethane reduces glutamate release to a much lesser extent, and the nonanesthetic 1,2-dichlorohexafluorocyclobutane does not reduce glutamate release. These findings support the hypothesis that the modulation of excitatory neurotransmission might be responsible, in part, for in vivo anesthetic action.     

Bispectral index does not correlate with observer assessment of alertness and sedation scores during 0.5% bupivacaine epidural anesthesia with nitrous oxide sedation

The bispectral index (BIS) has been used as a measure of the degree of sedation and level of hypnosis for IV hypnotics and sedatives, potent volatile anesthetics. We evaluated the effect of increasing concentrations of nitrous oxide (N2O) on BIS and compared it with the Observer's Assessment of Alertness and Sedation (OAA/S) scale in patients undergoing regional anesthesia. We studied 48 unpremedicated, ASA physical status I-II adult patients scheduled for lower extremity surgery under lumbar epidural anesthesia. N2O was given in oxygen to achieve measured end-tidal concentrations of 33%, 50%, and 67% N2O by a tight-fitting facemask, and each N2O concentration was maintained for 20 min. Paired measurements of BIS and OAA/S scores were obtained just before each increase in N2O concentration. Forty of the 48 subjects completed the study. Increasing N(2)O concentrations produced no changes in BIS despite a significant decrease in OAA/S scores at 50% and 67% N2O concentrations. The prediction probability for BIS and OAA/S calculated by Somers' d(x.y) were 0.60 and 0.84, respectively. Anesthesiologists should be aware that the BIS monitor may not be sensitive enough to provide an adequate measure of the depth of sedation and hypnosis when using N2O alone for sedation. It may be better to monitor sedation clinically (e.g., with the OAA/S scale) to determine the dose requirement and the adequacy of depth of sedation and hypnosis.