全身麻醉机制与下丘脑腹外侧视前核睡眠通路

背景 全身麻醉与自然睡眠之间存在一定的相似性,但睡眠-觉醒核团是否参与全身麻醉药物致意识消失的过程目前仍未有定论. 目的 综述睡眠-觉醒通路中主要的促睡眠核团下丘脑腹外侧视前核(ventrolateral preoptic nucleus,VLPO)及其相关通路与全身麻醉机制之间的关系. 内容 全身麻醉药可能会通过兴奋主要的促睡眠核团和抑制关键的促觉醒核团产生镇静催眠效应. 趋向 探讨全身麻醉药物作用于睡眠核团及其相关通路的生理机制,为全身麻醉机制研究提供一新的思路.     

丙泊酚的脑内作用区域研究进展

背景 丙泊酚作为目前临床应用中最重要的全身麻醉药之一,其麻醉作用机制至今尚未完全阐明,尤其是在脑内的功能性靶点研究目前还极其有限. 目的 探讨丙泊酚在脑内可能的靶点位置. 内容 分别阐述内源性睡眠下丘脑通路、网状上行激动系统、丘脑皮质网络以及丘脑网状核和丙泊酚麻醉机制可能存在的相关性. 趋向 揭示丙泊酚麻醉作用的始动核团抑或相关区域,对于避免过深和过浅麻醉所带来的不良后果、减少麻醉并发症以及更为有效的麻醉药物的开发都具有重要的指导意义.     

觉醒神经通路参与全身麻醉苏醒的研究进展

背景 大量的研究表明全身麻醉苏醒与觉醒有着相同的中枢神经通路,即在觉醒期表现活跃的脑区、大脑皮质及相关脑区增多的神经递质与全身麻醉苏醒期有着一致改变. 目的 总结分析上行觉醒神经系统在全身麻醉苏醒中的作用,为全身麻醉药物苏醒机制的进一步研究提供新的思路. 内容 主要从全身麻醉苏醒的简介、上行觉醒神经通路、觉醒神经通路参与全身麻醉苏醒等三方面就与此相关的研究进展作一系统的综述. 趋向 上行觉醒系统在全身麻醉苏醒机制中的关键作用将会被进一步关注与深入研究,为解决苏醒延迟导致的术后谵妄或术后认知功能障碍等问题提供新的线索.     

睡眠觉醒环路与全身麻醉机制研究进展

背景 全身麻醉与睡眠都表现为觉醒水平的降低,以及对外界环境刺激反应的抑制,二者具有相似的脑电图和局部脑功能变化.近年研究表明,全身麻醉药通过抑制脑内促觉醒神经核团和戚激活促睡眠神经核团发挥镇静催眠及意识消失作用.目的 从睡眠觉醒环路的角度综述全身麻醉神经机制的研究进展.内容 麻醉药诱导的意识消失与自然睡眠觉醒产生的机制并非完全相同,每种麻醉药物作用的靶神经核团也存在一定的差异.趋向 深入研究睡眠觉醒环路及全身麻醉神经机制,将有助于研发新型安全有效的麻醉剂.     

全身麻醉的重要核团——蓝斑核

正全身麻醉是由药物诱导的,可逆转的意识丧失状态。随着全麻药的研究从分子机制转型到神经网络,越来越多的研究发现内源性睡眠-觉醒系统及相关功能网络核团参与其中~([1])。研究麻醉诱导与复苏相关的神经网络核团,不仅有助于阐明意识丧失的神经网络机制,也有助于对麻醉复苏过程的深入理解。前期研究发现,下丘脑腹外侧视前区(ventrolateral preoptic nucleus,VLPO)与面旁核的GABA能神经元促进睡眠     

右美托咪定经鼻喷雾治疗术后睡眠障碍的效果

目的 观察右美托咪定经鼻喷雾治疗术后睡眠障碍的临床效果。
方法 选择全麻气管插管下行颌面外科手术患者78例，男12例，女66例，年龄18～40岁，ASAⅠ或Ⅱ级。将患者随机分为两组：对照组（C组）和右美托咪定组（D组），每组39例。术后当天21:30 C组和D组分别给予生理盐水0.01 ml/kg和右美托咪定1 μg/kg经鼻喷雾。采用多导睡眠监测仪（PSG）记录术后当天N1期、N2期、N3期、REM期睡眠时间、清醒时间、觉醒次数和睡眠效率。采用匹兹堡睡眠质量指数（PSQI）量表评估术前1个月及术后当天的睡眠情况。记录术后当天补救镇静镇痛情况。
结果 与C组比较，术后当天D组N2期睡眠明显延长（P＜0.05），清醒时间明显缩短（P＜0.05），觉醒次数明显减少（P＜0.05），睡眠效率明显提高（P＜0.05）。与术前1个月比较，术后当天两组PSQI总分明显升高（P＜0.05），与C组比较，术后当天D组PSQI总分明显降低（P<0.05）。术后当天两组补救镇静镇痛率差异无统计学意义。
结论 通过右美托咪定经鼻喷雾，可有效延长颌面外科手术患者术后当天的N2期睡眠，缩短清醒时间，减少觉醒次数，明显提高睡眠效率。     

星状神经节阻滞对腹腔镜全子宫切除术患者术后睡眠质量和恶心呕吐的影响

目的 观察超声引导下右侧星状神经节阻滞（SGB）对腹腔镜全子宫切除术患者术后睡眠质量和恶心呕吐（PONV）的影响。
方法 选择择期行腹腔镜全子宫切除术患者98例,年龄42～74岁,BMI 19～25 kg/m ²,ASAⅠ或Ⅱ级。采用随机数字表法分为两组：全身麻醉联合SGB组（S组）和全身麻醉组（GA组）,每组49例。S组于麻醉诱导前在超声引导下行右侧SGB,注入 0.2%罗哌卡因5 ml,GA组不行SGB。两组采用相同的全身麻醉方法和麻醉药物。记录术前1 d、手术当日、术后1 d的匹兹堡睡眠质量指数（PSQI）。记录术后24 h PONV分级和止吐药补救情况。记录术后24 h活动时VAS疼痛评分、镇痛药补救情况、术后首次下床活动时间和术后住院时间。记录局麻药中毒、全脊髓麻醉、气胸、臂丛神经阻滞等SGB相关并发症发生情况。
结果 与GA组比较,S组手术当日、术后1 d PSQI评分、POSD发生率明显降低（P＜0.05）,PONV 0级、1级发生率明显升高,PONV 2级、3级、4级发生率、止吐药补救率明显降低（P＜0.05）,术后24 h活动时VAS疼痛评分明显降低（P＜0.05）,术后首次下床活动时间明显缩短（P＜0.05）。两组补救镇痛情况、术后住院时间差异无统计学意义。S组无一例出现局麻药中毒、全脊髓麻醉、气胸、臂丛神经阻滞等SGB相关并发症。
结论 右侧星状神经节阻滞可有效改善腹腔镜全子宫切除术患者的术后睡眠质量,降低术后恶心呕吐的发生率及严重程度,减轻术后疼痛。     

不同镇痛方法用于髋部或股骨干骨折患者椎管内麻醉摆放体位时镇痛效果的网状Meta分析

目的 采用网状Meta分析系统评价不同镇痛方法用于髋部或股骨干骨折患者椎管内麻醉摆放体位时的镇痛效果。
方法 计算机检索PubMed、Cochrane Library、Web of Science、EMbase、中国生物医学文献数据库(CBM)、中国知网、维普、万方，检索时间为建库至2022年8月，纳入髋部或股骨干骨折患者摆放体位和椎管内麻醉时实施镇痛的随机对照研究。由两名研究员独立进行文献筛选、资料提取和偏倚风险评价，采用Stata 17.0和RevMan 5.3软件进行统计分析。
结果 共纳入28篇文献，患者1 773例。累计排序概率曲线下面积（SUCRA）显示，降低摆放体位时VAS疼痛评分PENG阻滞（94.4%）效果最佳，其次是FIB联合IVA（83.8%）和FIB（71.1%）；降低椎管内麻醉时VAS疼痛评分PENG阻滞（98.2%）效果最佳，其次是FIB（71.1%）和FNB（55.6%）；缩短椎管内麻醉操作时间PENG阻滞（84.1%）效果最佳，其次是FNB（70.7%）和FIB（68.5%）；升高体位摆放质量评分PENG阻滞（99.1%）效果最佳，其次是FIB（73.1%）和FNB（52.9%）。
结论 神经阻滞或神经阻滞联合IVA可降低髋部或股骨干骨折患者体位摆放和椎管内麻醉时VAS疼痛评分、缩短麻醉操作时间和升高体位摆放质量评分。PENG阻滞对髋部或股骨干骨折患者摆放体位和椎管内麻醉时实施镇痛的效果最佳。     

丘脑网状核在睡眠中的作用

背景 睡眠是脑的重要功能活动之一,是人类生存的必要条件.而γ-氡基丁酸(γ-aminobutyric acid,GABA)是中枢神经系统广泛分布的一种抑制性神经递质,睡眠以及全身麻醉的产生均与GABA存在密切的关系. 目的 综述丘脑皮质系统中富含GABA神经元的丘脑网状核(thalamic reticular nucleus,TRN)在睡眠中的作用. 内容 丘脑网状核可能会通过其抑制性闸门作用调节睡眠. 趋向 TRN及其参与的丘脑-皮质环路在睡眠中的相关生理机制为睡眠及相关全身麻醉研究提供了一新靶点.     

不同麻醉方式与老年患者髋关节置换术后转归的相关性

目的 比较不同麻醉方式对老年患者髋关节置换术后转归的影响。
方法 回顾性分析2012年12月至2018年10月行髋关节置换术患者566例,年龄≥75岁,根据麻醉方式分为两组：全身麻醉组（G组,n=233）和蛛网膜下腔阻滞组（S组,n=333）。采用倾向评分将患者按1∶1匹配,得到组间协变量均衡样本。比较两组术中情况、术后并发症、转入ICU例数和住院时间。
结果 对患者一般资料进行匹配后,G组和S组各纳入患者225例。与G组比较,S组手术时间、麻醉时间、手术室停留时间明显缩短,心血管并发症、肺部感染、深静脉血栓形成/肺栓塞、术后谵妄、术后恶心呕吐、转入ICU率明显降低,住院时间明显缩短,术后头痛、尿潴留发生率明显升高（P<0.05）。
结论 对于老年髋关节置换术患者,蛛网膜下腔阻滞可以改善术后转归,加速术后康复进程。     

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.     

在麻醉致意识消失期间丙泊酚和乙托咪酯对大脑皮质、丘脑及网状结构神经元的抑制作用

背景麻醉致意识消失的作用位点仍不清楚。可能的位点包括大脑皮质、丘脑和网状结构。我们研究了丙泊酚和乙托咪酯对正常动物皮质、丘脑及网状结构神经元功能的影响。方法对5只猫在麻醉状态下放置记录套管和脑电波螺丝钉电极。经过5天恢复期之后,每周重复检查3～4次。在给予丙泊酚或乙托咪酯注射之前、注射期间和注射之后记录大脑皮质（7、18和19区）、丘脑（腹后外侧核、腹后内侧核和内侧膝状体）及网状结构（中脑网状核群和中央被盖区）单个神经元的电活动。皮质神经元的动作电位按脉冲神经元和快速放电神经元分别进行分析。结果丙泊酚和乙托咪酯使皮质神经元自发放电频率降低37％-41％。两种麻醉剂对脉冲神经元和快速放电神经元的作用相似。丙泊酚和乙托咪酯亦使丘脑和网状结构神经元放电频率减低30％～49％。麻醉剂输注期间皮质、丘脑及网状结构脑电图表现相似,均从低幅高频快波变为高幅低频慢波;功率峰值发生于丙泊酚输注期间,频率为12～13Hz。乙托咪酯麻醉期间有2个大的峰值：一个频率为12—14Hz,另一个为7～8Hz。检测过程中猫处于深度镇静状态,瞬目反射和动须反射消失而伤害性刺激}】起的退缩反应保存。结论数据资料显示丙泊酚和乙托咪酯抑制大脑皮质、丘脑及网状结构神经元的作用相似。尽管麻醉剂对神经元电活动的抑制作用可能是麻醉剂致意识消失的潜在机制,但仍需进一步研究阐明上述位点的麻醉剂效应如何相互影响而终致意识消失。     

Sleep and general anesthesia

Purpose

The mechanisms through which general anesthetics cause reversible loss of consciousness are characterized poorly. In this review, we examine the evidence that anesthetic-induced loss of consciousness may be caused by actions on the neuronal pathways that produce natural sleep.

Principal findings

It is clear that many general anesthetics produce effects in the brain (detected on electroencephalogram recordings) that are similar to those seen during non-rapid eye movement non-(REM) sleep. Gamma aminobutyric acid (GABA)ergic hypnogenic neurons are thought to be critical for generating non-REM sleep through their inhibitory projections to wake-active regions of the brain. The postsynaptic GABA_A receptor is a major molecular target of many anesthetics and thus may be a point of convergence between natural sleep and anesthesia. Furthermore, we also present growing evidence in this review that modulating wake-active neurotransmitter (e.g., acetylcholine, histamine) release can impact on anesthesia, supporting the idea that this point of convergence is at the level of the brain arousal systems.

Conclusions

While it is clear that general anesthetics can have effects at various points in the sleep-wake circuitry, it remains to be seen which points are true anesthetic targets. It will be challenging to separate non-specific effects on baseline arousal from a causal mechanism. Sophisticated experimental approaches are necessary to address basic mechanisms of sleep and anesthesia and should advance our understanding in both of these fields.     

Interfaces of sleep and anesthesia

In the past decades there has been an increasing focus on the relationship of sleep and anesthesia. This relationship bears on the fundamental scientific questions in anesthesiology, such as the mechanism of anesthetic-induced unconsciousness. However, given the increasing prevalence of sleep disorders in surgical patients, the interfaces of sleep and anesthesia are now a pressing clinical concern. This article discusses sleep and anesthesia from the perspective of phenotype, mechanism and function, with some concluding thoughts on the relevance to neuroanesthesiology.     

Sleep and anesthesia--part 2, on the relationship between sleep and general anesthesia

We reviewed historical and current trends on study regarding the relationship between sleep and general anesthesia. Historically, sleep has been recognized as a completely different physiological phenomenon from general anesthesia. Therefore, sleep study has been thought that it has no merit in anesthesia study. However, on the basis of recent evidence, sleep may share some part of its mechanism with general anesthesia; thus, studies focusing sleep mechanism may also contribute to elucidate some mechanism of general anesthesia. Moreover, research to solve anesthesia related-sleep disorder would be useful to improve patient's quality of life and save much medical resource.     

Hypoxia-induced Vasoconstriction in Isolated Perfused Lungs exposed to Injectable or Inhalation Anesthetics

Investigations during the last two decades have revealed a tendency to impaired pulmonary gas exchange in patients during general anesthesia. In the awake state, arterial hypoxemia is counteracted by a mechanism which tends to normalize the ventilation perfusion ratio of the lungs by way of a hypoxia-induced vasoconstriction in poorly ventilated areas. This results in a redistribution of perfusion to more adequately ventilated lung regions. Recent observations suggest, however, that this beneficial mechanism is blunted by some commonly used inhalation anesthetics.
In the present study the effects of inhalation anesthetics and injectable anesthetics on the vasoconstrictor response to acute alveolar hypoxia have been compared in isolated blood-perfused rat lungs. The experiments showed that the response was unaffected by N₂O and injectable anesthetics, while a reversible, dose-dependent damping effect was demonstrated for the volatile inhalation anesthetics, ether, halothane and methoxyflurane. The effect could be demonstrated at blood concentrations comparable to those used in clinical anesthesia, and it was not due to a general paralysis of the vascular smooth muscle. The findings might, at least in part, explain the occurrence of arterial hypoxemia during general inhalation anesthesia.     

Interactions between general and regional anesthesia

Neuraxial blockade is commonly used to abolish sensations elicited by noxious stimuli during surgical procedures. Proven advantages of combined anesthesia include early recovery from general anesthesia and postoperative analgesia, together with likely decreases in blood loss, cardiac dysrhythmias, or ischemic events and postoperative deep vein thrombosis. The side effects of the technique are related to the dose or site of local anesthetic administration and to light general anesthesia, which can result in awareness during surgery. Varying degrees of synergistic interactions have been reported among the drugs used to achieve the anesthetic state. Spinal anaesthesia appears to have sedative effects, and local anesthetics used for neuraxial blockade have been found to reduce the induction and maintenance dosage of midazolam, thiopental, propofol and inhaled anesthetics. The growing interest in combining local and general anesthesia has led to studies investigating possible interactions between general anesthesia and local anesthetics administered via spinal or epidural routes. Neuraxial blockade reduces sedative and anesthetic requirements by decreasing ascending sensory input into the brain. This has important clinical implications, as anesthetists should expect to reduce anesthetic and sedative drug doses during neuraxial blockade, unless the blockade involves lower dermatomes alone. Clinical practice of anesthesia is a polypharmacy, wherein the anesthetic state is the net result of the action of different drugs and their interaction in the presence of a surgical stimulus.