第一年3篇文献

1、Consciousness and General AnaesthesiaConsciousness can be defined as explicit awareness. Awareness impst thebrain is aroused andtrson has specific perceptual qualities of an experience (e.g.,a hot chocolate drink). The term “explicit” distinguishes conscious awareness fromcognitive proseshe brahat a

2、re implicit or unconscious. Explicit awareness doesnot nesarily implyt the patient will also have explicit recall, for exle the recallof a surgicalervention. The key anatomic structures of the central nervous system(CNS)lamus (t contribute to the se of consciousness are: the brain stem, the pons, th

3、e lamic nuclei) and the brain cortex with their connecting neural pathways.1. Molecular and cellular actions of general anaestheticsThere are two types of general anaesthetics: (a)ravenous agents (e.g., propofol),generally administered together with sedatives or narcotics and (b) volatile agents (e.

4、g.,sevoflurane). Both types of anaesthetics modulate the permeability of ion channelstregulate synaptic transmisand membrane potentials in key regions of the CNS. Allgeneral anaesthetic agents are relatively apolar, to be able to cross the blood-brain barrier,anderact with their(i.e., receptor) thro

5、ugh weak polarization forandhydrogen bonding . The binding of a general anaesthetic to its receptor leads to neuronhypolarisation due to increased inhibition or to decreased exciion thus alteringneuronal activity.The actions of a general anaesthetic on the molecular level are reflected on the brains

6、 electrical activity as a transition from the low voltage, high-frequency pattern ofwakefulness (known aivated EEG), to the slow-wave EEG of the deep, non-raeyemovement (NREM) sleep, and finally to an EEG burst-supprespattern. General-aminobutyric acid receptors(e.g.,anaesthetics act on differents,

7、i.e., receptors, for exle(GABA)typeA,nicotinicacetylcholine,andglutamateN-methyl-D-aspare receptors) in the brain, as well as glycine receptors in the spinalcord. A clear distinction has to be made betn the actions of general anaesthetics andthe mechanism of general anaesthesia. The actions of gener

8、al anaesthetics on the brainreceptors are well known; the pros by which these actions translateo generalanaesthesia (i.e., the mechanism of general anaesthesia) is not wel2. The anaesthetised patientderstood.The initial signs of GA (stage 1 anaesthesia) can be a se similar to drunkenness, gesia (the

9、 inability to feel pain while still conscious), amnesia (loss of memory),distorted time perception or increased sle fails to move in response to a verbalness. With higher anaesthetic doses, a patient d and is considered to be unconscious.However, unresponsiveness during GA can occur without unconsci

10、ousness. For exle,paralyzing agents used to prevent unwanted movements during anaesthesia do not remove consciousness. Most general anaesthetics will cause a global deactivation of the brain athigher doses. The exceptions are dissotive anaesthetics, like,t increase induced changes in anaesthetised p

11、atient.global brain metabolism, espelly in thelamus. Theglobal brain metabolism are reflected in the responsesof thecauses loss of motivation to followdsower doses; at higher dosescauses a characteristic se in which the eyes are open and the face takes on adisconnected blstare consistent with the de

12、activation of executive circuits in anteriorcingulate cortex and basal ganglia.At doses near the unconsciousness threshold, some anaesthetics block working memory and patients may fail to respond because theyimmediay fet what to do. Also, some patients under general anaesthesia can carry ona convers

13、ation using hand signals, buttoperatively deny ever being awake during thesurgical procedure. Surgery is performed when the patient is perceived to reach stage 3 general anaesthesia. Increasing doses of modern general anaesthetics (i.e., an overdose)do not cause brain death directly but lead tosatio

14、n of spontaneous ventilation andimpairment of cardiovascular function (stage 4 anaesthesia). This stage is le l without proper cardiovascular and respiratory support, which is standard in a modern operating theater.Therefore, monitoring the DGA is essential to tailor the optimal dose of generalanaes

15、thetic to the individual patient thus reducing the incidence ofraoperativeawareness or preventing the effects of an overdose of general anaesthetic. Although there are several“brain-function monitors” available they have a limited ability to detectdirectly the presence or absence of consciousness, e

16、spe when loss of consciousness occurs .lly around the transition poKey word: Consciousness，general anaesthetics，awareness意识和全身麻醉意识可以被定义为明确的认知。意识意味着大脑被调动和一个人对一段经历有明确的感知（例如，一杯热巧克力）。所谓“明确”区分自觉意识和大脑的认知过程是隐含的或无意识的自觉意识。清楚的认知，并不一定意味着该患者也将有明确的回忆，例如手术干预的回忆。中枢神经系统与意识状态相关的关键解剖结构（CNS）的有：脑干，脑桥，丘脑（丘脑核）和脑皮质及与其连接的神

17、经通路。1. 全身的分子和细胞作用有两种类型的全身麻醉剂：（1）静脉（如丙泊酚），一般与剂或麻醉剂和（b）挥发性药物（例如，七氟醚）一起使用。这两种类型的麻醉剂通过调节离子通道的渗透性从而调节中枢神经系统中关键区域的突触传递和膜电位。所有全身麻醉剂是相对非极性的，以便能够穿越血-脑屏障，并通过弱极化力和氢键键合与它们的靶（即受体）相互作用。全身麻醉与其受体的结合导致了神经元的超极化，由于增加的抑制或降低兴奋性从而改变神经元活动。在分子水平上全身物的作用反映在大脑电活动为从低电压高频形式的觉醒（称为活化的脑电图）过渡到深慢波脑电图，非快速动眼（NREM）睡眠，并最终到脑电图爆发抑制形式。全身麻醉

18、剂作用于不同的靶标，即，受体，例如 在大脑中氨基丁酸（GABA）A 型，乙酰胆碱和谷氨酸受体（例如，N-甲基-D-氨酸受体），以及在脊髓中的甘氨酸受体。全身物的作用和全身麻醉的机制之间是有明显区别的。全身物对大脑受体的作用是众所周知的;这一作用是如何转化为全身麻醉（即，全身麻醉的机制）目前并不清楚。2.麻醉GA（阶段 1 麻醉）的最初症状类似醉酒的状态，镇痛（清醒却无法感觉到疼痛，），健忘（缺失），的时间感知或嗜睡加重。在较高麻醉剂量时，对一个口头指令没有办法移动，就被认为是无意识的。然而，GA 时反应迟钝时可发生在神志清醒时。例如，麻痹药物用来防止麻醉过程中不必要的动作，而不能让无意识。大多数的麻醉剂将在较高剂量导致脑的全部失活。例外的是游离性麻醉剂，如，增加全脑代谢，特别是在丘脑。引起的全脑代谢变化体现在麻醉病人的反应上。在低剂量时引起对指令的制动;在较高剂量时引起的特征性状态，其中双眼睁开，脸部呈现两眼发直的状态，这与执行回路的前扣带皮质和基底神经节失活是一致的。一些在剂量接近使患者无