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Dowd, Noreen P., Davy C. H. Cheng, Jacek M. Karski, David T. Wong, Jo A. Carroll Munro, and Alan N. Sandler. "Intraoperative Awareness in Fast-track Cardiac Anesthesia." Anesthesiology 89, no. 5 (1998): 1068–73. http://dx.doi.org/10.1097/00000542-199811000-00006.
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Background Fast-track cardiac anesthesia, using low-dose narcotics combined with short-acting anesthetic and sedative agents, facilitates early tracheal extubation after cardiac surgery. The incidence of awareness with this anesthetic technique has not been investigated previously. The purpose of this study was to prospectively investigate the incidence of intraoperative awareness with explicit memory of events during fast-track cardiac anesthesia. Methods Data were collected prospectively over a 4-month period from 617 consecutive adult patients undergoing cardiac surgery at a university hospital. All patients received a fast-track cardiac anesthetic regimen. Patients underwent a structured interview by a research nurse 18 h after extubation. A standard set of questions was asked during this interview to determine if the patient had explicit memory of any event from induction of anesthesia to recovery of consciousness. Results Nine patients did not complete a postoperative interview because of death (n = 7) or postoperative confusion (n = 2). The last memory before surgery reported in 420 (69.1%) patients was waiting in the holding area at the operating suite, and in the remaining 188 (30.9%) patients it was lying on the operating table before induction of anesthesia. Two patients (0.3%) had explicit memory of intraoperative events. One of the two patients also had explicit memory of pain. Neither patient reported adverse psychological sequelae. Conclusions The authors report an incidence of awareness in fast-track cardiac anesthesia of 0.3%. This is the lowest incidence of awareness currently reported during cardiac surgery. This low incidence of awareness may be related to the use of a balanced anesthetic technique involving the continuous administration of volatile (isoflurane) or intravenous (propofol) anesthetic agents before, during, and after cardiopulmonary bypass.
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Martin, Loren J., Gabriel H. T. Oh та Beverley A. Orser. "Etomidate Targets α5γ-Aminobutyric Acid Subtype A Receptors to Regulate Synaptic Plasticity and Memory Blockade". Anesthesiology 111, № 5 (2009): 1025–35. http://dx.doi.org/10.1097/aln.0b013e3181bbc961.
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Background The memory-blocking properties of general anesthetics have recently received considerable attention because of concerns related to intraoperative awareness and postoperative cognitive dysfunction. The goal of this study was to identify the mechanisms by which gamma-aminobutyric acid subtype A receptors that contain the alpha5 subunit (alpha5GABAARs) induce memory-blockade by etomidate and a pharmacologic strategy to reverse this impairment. Methods The effects of etomidate and the alpha5GABAAR-preferring inverse agonist L-655,708 on the plasticity of glutamatergic excitatory transmission in hippocampal slices and behavioral memory for spatial navigational and fear-associated memory tasks were studied in wild-type and null mutant mice for the gene that encodes the alpha5 subunit (Gabra5-/- mice). Long-term potentiation of field excitatory postsynaptic potentials was induced in CA1 pyramidal neurons following high-frequency stimulation of Schaffer collaterals. Memory performance was studied in contextual, cued, and trace fear conditioning assays and the Morris water maze. Results Robust synaptic plasticity induced by high-frequency stimulation and memory performance for contextual fear and spatial navigational memory were not influenced by a decrease in the function of alpha5GABAARs. Nevertheless, etomidate, via an increase in alpha5GABAAR activity, completely blocked long-term potentiation and impaired memory performance, and these effects were reversed by pretreatment with L-655,708. Conclusions The results provide the first proof of concept that memory blockade by a general anesthetic can be reversed by inhibiting the function of alpha5GABAARs. The findings suggest a mechanism and model for awareness during anesthesia.
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Sleigh, Jamie W., Kate Leslie, Andrew J. Davidson, et al. "Genetic Analysis of Patients Who Experienced Awareness with Recall while under General Anesthesia." Anesthesiology 131, no. 5 (2019): 974–82. http://dx.doi.org/10.1097/aln.0000000000002877.
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Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Intraoperative awareness with recall while under apparently adequate general anesthesia is a rare, unexplained, and often very distressing phenomenon. It is possible that a relatively small number of genetic variants might underlie the failure of general anesthetic drugs to adequately suppress explicit memory formation and recall in the presence of apparently adequate anesthesia concentrations. Methods The authors recruited 12 adult patients who had experienced an episode of intraoperative awareness with recall (compared with 12 controls), performed whole exome sequencing, and applied filtering to obtain a set of genetic variants that might be associated with intraoperative awareness with recall. The criteria were that the variant (1) had a minor allele frequency less than 0.1% in population databases, (2) was within exonic or splicing regions, (3) caused a nonsynonymous change, (4) was predicted to be functionally damaging, (5) was expressed in the top 50% of genes expressed in the brain, and (6) was within genes in Kyoto Encyclopedia of Genes and Genomes pathways associated with general anesthesia, drug metabolism, arousal, and memory. Results The authors identified 29 rare genetic variants in 27 genes that were absent in controls and could plausibly be associated with this disorder. One variant in CACNA1A was identified in two patients and two different variants were identified in both CACNA1A and CACNA1S. Of interest was the relative overrepresentation of variants in genes encoding calcium channels and purinergic receptors. Conclusions Within the constraints of the filtering process used, the authors did not find any single gene variant or gene that was strongly associated with intraoperative awareness with recall. The authors report 27 candidate genes and associated pathways identified in this pilot project as targets of interest for future larger biologic and epidemiologic studies.
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Hauer, Daniela, Patrizia Ratano, Maria Morena, et al. "Propofol Enhances Memory Formation via an Interaction with the Endocannabinoid System." Anesthesiology 114, no. 6 (2011): 1380–88. http://dx.doi.org/10.1097/aln.0b013e31821c120e.
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Background Propofol is associated with postoperative mood alterations and induces a higher incidence of dreaming compared with other general anesthetics. These effects might be mediated by propofol's inhibitory action on fatty acid amide hydrolase, the enzyme that degrades the endocannabinoid anandamide. Because propofol is also associated with a higher incidence of traumatic memories from perioperative awareness and intensive care unit treatment and the endocannabinoid system is involved in regulating memory consolidation of emotional experiences, the authors investigated whether propofol, at anesthetic doses, modulates memory consolidation via an activation of the endocannabinoid system. Methods Male Sprague-Dawley rats were trained on an inhibitory avoidance task in which they received an inescapable foot shock upon entering the dark compartment of the apparatus. Drugs were administered intraperitoneally immediately or 30, 90, or 180 min after training. On the retention test 48 h later, the latency to reenter the dark compartment was recorded and taken as a measure of memory retention. Results The anesthetic doses of propofol administered after training significantly increased latencies of 48-h inhibitory avoidance performance (483.4 ± 181.3, 432.89 ± 214.06, 300 and 350 mg/kg, respectively; mean ± SD) compared with the corresponding vehicle group (325.33 ± 221.22, mean ± SD), which is indicative of stronger memory consolidation in propofol treated rats. Administration of a nonimpairing dose of the cannabinoid receptor antagonist rimonabant blocked the memory enhancement induced by propofol (123.39 ± 133.10, mean ± SD). Delayed administration of propofol 90 and 180 min after training or immediate posttraining administration of the benzodiazepine midazolam or the barbiturate pentobarbital did not significantly alter retention. Conclusions These findings indicate that propofol, in contrast to other commonly used sedatives, enhances emotional memory consolidation when administered immediately after a stressful event by enhancing endocannabinoid signaling.
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Guerra, Frank. "Memory and Awareness in Anesthesia." Anesthesia & Analgesia 71, no. 5 (1990): 571???572. http://dx.doi.org/10.1213/00000539-199011000-00034.
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EICH, E., I. L. REEVES, and R. L. KATZ. "Anesthesia, Amnesia, and the Memory/Awareness Distinction." Survey of Anesthesiology 30, no. 3 (1986): 128. http://dx.doi.org/10.1097/00132586-198606000-00021.
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Eich, Eric, John L. Reeves, and Ronald L. Katz. "Anesthesia, Amnesia, and the Memory/Awareness Distinction." Anesthesia & Analgesia 64, no. 12 (1985): 1143???1148. http://dx.doi.org/10.1213/00000539-198512000-00002.
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Gaya da Costa, Mariana, Alain F. Kalmar, and Michel M. R. F. Struys. "Inhaled Anesthetics: Environmental Role, Occupational Risk, and Clinical Use." Journal of Clinical Medicine 10, no. 6 (2021): 1306. http://dx.doi.org/10.3390/jcm10061306.
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Inhaled anesthetics have been in clinical use for over 150 years and are still commonly used in daily practice. The initial view of inhaled anesthetics as indispensable for general anesthesia has evolved during the years and, currently, its general use has even been questioned. Beyond the traditional risks inherent to any drug in use, inhaled anesthetics are exceptionally strong greenhouse gases (GHG) and may pose considerable occupational risks. This emphasizes the importance of evaluating and considering its use in clinical practices. Despite the overwhelming scientific evidence of worsening climate changes, control measures are very slowly implemented. Therefore, it is the responsibility of all society sectors, including the health sector to maximally decrease GHG emissions where possible. Within the field of anesthesia, the potential to reduce GHG emissions can be briefly summarized as follows: Stop or avoid the use of nitrous oxide (N2O) and desflurane, consider the use of total intravenous or local-regional anesthesia, invest in the development of new technologies to minimize volatile anesthetics consumption, scavenging systems, and destruction of waste gas. The improved and sustained awareness of the medical community regarding the climate impact of inhaled anesthetics is mandatory to bring change in the current practice.
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Yang, Wei, Mattia Chini, Jastyn A. Pöpplau, et al. "Anesthetics fragment hippocampal network activity, alter spine dynamics, and affect memory consolidation." PLOS Biology 19, no. 4 (2021): e3001146. http://dx.doi.org/10.1371/journal.pbio.3001146.
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General anesthesia is characterized by reversible loss of consciousness accompanied by transient amnesia. Yet, long-term memory impairment is an undesirable side effect. How different types of general anesthetics (GAs) affect the hippocampus, a brain region central to memory formation and consolidation, is poorly understood. Using extracellular recordings, chronic 2-photon imaging, and behavioral analysis, we monitor the effects of isoflurane (Iso), medetomidine/midazolam/fentanyl (MMF), and ketamine/xylazine (Keta/Xyl) on network activity and structural spine dynamics in the hippocampal CA1 area of adult mice. GAs robustly reduced spiking activity, decorrelated cellular ensembles, albeit with distinct activity signatures, and altered spine dynamics. CA1 network activity under all 3 anesthetics was different to natural sleep. Iso anesthesia most closely resembled unperturbed activity during wakefulness and sleep, and network alterations recovered more readily than with Keta/Xyl and MMF. Correspondingly, memory consolidation was impaired after exposure to Keta/Xyl and MMF, but not Iso. Thus, different anesthetics distinctly alter hippocampal network dynamics, synaptic connectivity, and memory consolidation, with implications for GA strategy appraisal in animal research and clinical settings.
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Felipe, Bianca, Sofia Chane, Antonio De Mello, and Gabriela Mayrink. "Knowledge of Dental Students in Relation to Local Anesthetics and Associated Complications." International Journal of Medical and Surgical Sciences 2, no. 2 (2018): 461–67. http://dx.doi.org/10.32457/ijmss.2015.013.
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Local anesthesia is the most frequently performed procedure for all dentists and, despite their possible complications, often aspects such as dosage, contraindications and systemic effects are neglected. The objectives of this study are to evaluate prospectively the knowledge of undergraduate students for the technical, dosage and indication of local anesthetics in daily dental practice, in addition to clinical observation of possible complications from anesthesia. Questionnaires were distributed to students asking about the procedure undertaken, anesthetic volume used, because of the choice of the anesthetic, anesthetic dosage calculation, habit of relating the patient's weight dosage with the dosage being applied, habit of observing the reflux in cartridge in the anesthetic infiltration act and adverse effects on patients, type of anesthetic technique performed and expected time to onset of action of the drug. At the end of this study, we intend to be a greater awareness of students (undergraduates) about the systemic effects of local anesthetics in patients, and possibly decrease the expenses of the institution with excessive use of anesthetic cartridges arising from incorrect anesthetic technique. The vast majority of undergraduate students have no knowledge about the type of anesthesia to be used, the amount to be administered and the anesthetic action time. The awareness of students about the dosage of anesthetics and their systemic problems, reduces waste and the cost of the institution by the indiscriminate use of anesthetics, therebycontributing to improve the clinical management of students at graduation.
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Pollard, Richard J., Joseph P. Coyle, Richard L. Gilbert, and Janet E. Beck. "Intraoperative Awareness in a Regional Medical System." Anesthesiology 106, no. 2 (2007): 269–74. http://dx.doi.org/10.1097/00000542-200702000-00014.
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Background Intraoperative awareness in patients undergoing general anesthesia is an infrequent but well-described adverse outcome. The reported incidence of this phenomenon is between 0.1% and 0.9%. Methods With institutional review board approval, the authors reviewed continuous quality improvement data from 3 yr (2002-2004) at the locations where the physician group provided anesthesia. Board-certified anesthesiologists supervising certified registered nurse anesthetists in the anesthesia care team model of practice delivered all anesthetics. Brain function monitors were not used in the operating room setting. Patients were interviewed twice during a 48-h postoperative period and, as part of that process, underwent a modified Brice interview to determine intraoperative awareness. All cases that met the criteria for awareness were examined by the continuous quality improvement committee to modify anesthetic practice and were included in this study. Results Data from 211,842 patients undergoing anesthesia were considered. Of these, the continuous quality improvement process followed up 177,468 (83.1%). Cases were not included in the study if the patient was younger than 18 yr, did not have a general anesthetic, or had a terminal event during the hospital course. By these criteria, a total of 87,361 patients followed by the continuous quality improvement process were at risk for awareness. Six patients reported instances of recall. Conclusion The incidence of intraoperative awareness in this large sample of patients from a regional medical center undergoing general anesthesia was 0.0068%, or 1 per 14,560 patients, substantially less than that reported in the recent literature.
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Wang, Fuzhou. "Is It Feasible of Prophylactic Alpha-5 GABA(A) Receptor Blockade for Preventing POCD?" Science Insights 3, no. 3 (2013): 61–62. http://dx.doi.org/10.15354/si.13.rp011.
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GAMMA-AMINOBUTYRIC ACID (GABA) is the chief inhibitory neurotransmitter in the mammalian central nervous system (CNS). It plays a role in regulating neuronal excitability throughout the nervous system. Also GABA activation is considered as the basis of general anesthesia including intravenous and inhalational anesthetics. Meanwhile, cumulating evidence indicated that GABA is the underlying mechanism of post-operative cognitive dysfunction (POCD). Based on these findings, researchers are beginning to focus on GABA as the target to treat POCD, but they ignored the role of GABA in the performance of general anesthesia, especially when the blockade of GABA was given prior to surgery. It is undoubtedly risking our patients in intra-operative awareness. Our exploratory data also verified our hypothesis in which the GABA inhibition would reduce the efficacy of inhalational anesthetics.
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Cascella, Marco, Vincenzo Schiavone, Maria Rosaria Muzio, and Arturo Cuomo. "Consciousness fluctuation during general anesthesia: a theoretical approach to anesthesia awareness and memory modulation." Current Medical Research and Opinion 32, no. 8 (2016): 1351–59. http://dx.doi.org/10.1080/03007995.2016.1174679.
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Jevtovic-Todorovic, Vesna. "Exposure of Developing Brain to General Anesthesia." Anesthesiology 128, no. 4 (2018): 832–39. http://dx.doi.org/10.1097/aln.0000000000002047.
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Abstract Recently, the U.S. Food and Drug Administration issued an official warning to all practicing physicians regarding potentially detrimental behavioral and cognitive sequelae of an early exposure to general anesthesia during in utero and in early postnatal life. The U.S. Food and Drug Administration concern is focused on children younger than three years of age who are exposed to clinically used general anesthetics and sedatives for three hours or longer. Although human evidence is limited and controversial, a large body of scientific evidence gathered from several mammalian species demonstrates that there is a potential foundation for concern. Considering this new development in public awareness, this review focuses on nonhuman primates because their brain development is the closest to humans in terms of not only timing and duration, but in terms of complexity as well. The review compares those primate findings to previously published work done with rodents.
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Hawkins, Joy L., Lisa M. Koonin, Susan K. Palmer, and Charles P. Gibbs. "Anesthesia-related Deaths during Obstetric Delivery in the United States, 1979–1990." Anesthesiology 86, no. 2 (1997): 277–84. http://dx.doi.org/10.1097/00000542-199702000-00002.
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Background Anesthesia-related complications are the sixth leading cause of pregnancy-related death in the United States. This study reports characteristics of anesthesia-related deaths during obstetric delivery in the United States from 1979-1990. Methods Each state reports deaths that occur within 1 yr of delivery to the Centers for Disease Control and Prevention as part of the ongoing Pregnancy Mortality Surveillance. Maternal death certificates (with identifiers removed) matched with live birth or fetal death certificates when available from 1979-1990 were reviewed to identify deaths due to anesthesia, the cause of death, the procedure for delivery, and the type of anesthesia provided. Maternal mortality rates per million live births were calculated. Case fatality rates and risk ratios were computed to compare general to regional anesthesia for cesarean section deliveries. Results The anesthesia-related maternal mortality rate decreased from 4.3 per million live births in the first triennium (1979-1981) to 1.7 per million in the last (1988-1990). The number of deaths involving general anesthesia have remained stable, but the number of regional anesthesia-related deaths have decreased since 1984. The case-fatality risk ratio for general anesthesia was 2.3 (95% confidence interval [CI], 1.9-2.9) times that for regional anesthesia before 1985, increasing to 16.7 (95% CI, 12.9-21.8) times that after 1985. Conclusions Most maternal deaths due to complications of anesthesia occurred during general anesthesia for cesarean section. Regional anesthesia is not without risk, primarily because of the toxicity of local anesthetics and excessively high regional blocks. The incidence of these deaths is decreasing, however, and deaths due to general anesthesia remain stable in number and hence account for an increased proportion of total deaths. Heightened awareness of the toxicity of local anesthetics and related improvements in technique may have contributed to a reduction in complications of regional anesthesia.
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Hernandez-Meza, Gabriela, Meltem Izzetoglu, Mary Osbakken, Michael Green, and Kurtulus Izzetoglu. "Near-Infrared Spectroscopy for the Evaluation of Anesthetic Depth." BioMed Research International 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/939418.
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The standard-of-care guidelines published by the American Society of Anesthesiologists (ASA) recommend monitoring of pulse oximetry, blood pressure, heart rate, and end tidal CO2during the use of anesthesia and sedation. This information can help to identify adverse events that may occur during procedures. However, these parameters are not specific to the effects of anesthetics or sedatives, and therefore they offer little, to no, real time information regarding the effects of those agents and do not give the clinician the lead-time necessary to prevent patient “awareness.” Since no “gold-standard” method is available to continuously, reliably, and effectively monitor the effects of sedatives and anesthetics, such a method is greatly needed. Investigation of the use of functional near-infrared spectroscopy (fNIRS) as a method for anesthesia or sedation monitoring and for the assessment of the effects of various anesthetic drugs on cerebral oxygenation has started to be conducted. The objective of this paper is to provide a thorough review of the currently available published scientific studies regarding the use of fNIRS in the fields of anesthesia and sedation monitoring, comment on their findings, and discuss the future work required for the translation of this technology to the clinical setting.
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Perouansky, Misha, Vinuta Rau, Tim Ford та ін. "Slowing of the Hippocampal θ Rhythm Correlates with Anesthetic-induced Amnesia". Anesthesiology 113, № 6 (2010): 1299–309. http://dx.doi.org/10.1097/aln.0b013e3181f90ccc.
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Background Temporary, antegrade amnesia is one of the core desirable endpoints of general anesthesia. Multiple lines of evidence support a role for the hippocampal θ rhythm, a synchronized rhythmic oscillation of field potentials at 4-12 Hz, in memory formation. Previous studies have revealed a disruption of the θ rhythm at surgical levels of anesthesia. We hypothesized that θ-rhythm modulation would also occur at subhypnotic but amnestic concentrations. Therefore, we examined the effect of three inhaled agents on properties of the θ rhythm considered critical for the formation of hippocampus-dependent memories. Methods We studied the effects of halothane and nitrous oxide, two agents known to modulate different molecular targets (GABAergic [γ-aminobutyric acid] vs. non-GABAergic, respectively) and isoflurane (GABAergic and non-GABAergic targets) on fear-conditioned learning and θ oscillations in freely behaving rats. Results All three anesthetics slowed θ peak frequency in proportion to their inhibition of fear conditioning (by 1, 0.7, and 0.5 Hz for 0.32% isoflurane, 60% N2O, and 0.24% halothane, respectively). Anesthetics inconsistently affected other characteristics of θ oscillations. Conclusions At subhypnotic amnestic concentrations, θ-oscillation frequency was the parameter most consistently affected by these three anesthetics. These results are consistent with the hypothesis that modulation of the θ rhythm contributes to anesthetic-induced amnesia.
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Kerssens, Chantal, Gitta H. Lubke, Jan Klein, Andries van der Woerd, and Benno Bonke. "Memory Function during Propofol and Alfentanil Anesthesia." Anesthesiology 97, no. 2 (2002): 382–89. http://dx.doi.org/10.1097/00000542-200208000-00015.
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Background Conscious recall and implicit memory have been shown to depend on hypnotic state as measured by electroencephalographic (EEG) bispectral index (BIS). A third expression of memory (unconscious-controlled memory) was recently observed after moderate to light sedation (BIS, 70-80). The present study investigated memory function during deep sedation (BIS, 60-70). As memory effects are small, the authors studied potential predictors of individual differences in memory performance. Methods Memory function and speed of information processing were assessed in 56 outpatients before surgery. During propofol anesthesia supplemented with alfentanil, patients heard a series of words while anesthesia was titrated to BIS, 60-70. In between words, response to command was assessed using the Isolated Forearm Technique. The authors tested memory with a word stem completion task and process dissociation procedure to distinguish explicit from implicit effects. Results Mean (+/- SD) BIS during word presentation was 64.0 +/- 3. Patients with conscious recall of verbal commands (n = 9) did not recall or recognize presented words. Even so, the process dissociation procedure revealed evidence of memory by a significantly higher hit rate in the inclusion condition (0.26) than in the exclusion condition (0.12). Patients without conscious recall showed no evidence of memory for presented words. Hit scores correlated significantly with scores in the preoperative memory test (r = 0.35). Conclusions The authors found evidence of weak explicit memory function during anesthesia titrated to BIS, 60-70. The observations strongly suggest that postoperative memory relates to awareness during anesthesia, but the nature of this relation remains unclear. Memory seems more likely in patients with good preoperative memory performance.
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Hao, Xuechao, Mengchan Ou, Donghang Zhang, et al. "The Effects of General Anesthetics on Synaptic Transmission." Current Neuropharmacology 18, no. 10 (2020): 936–65. http://dx.doi.org/10.2174/1570159x18666200227125854.
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General anesthetics are a class of drugs that target the central nervous system and are widely used for various medical procedures. General anesthetics produce many behavioral changes required for clinical intervention, including amnesia, hypnosis, analgesia, and immobility; while they may also induce side effects like respiration and cardiovascular depressions. Understanding the mechanism of general anesthesia is essential for the development of selective general anesthetics which can preserve wanted pharmacological actions and exclude the side effects and underlying neural toxicities. However, the exact mechanism of how general anesthetics work is still elusive. Various molecular targets have been identified as specific targets for general anesthetics. Among these molecular targets, ion channels are the most principal category, including ligand-gated ionotropic receptors like γ-aminobutyric acid, glutamate and acetylcholine receptors, voltage-gated ion channels like voltage-gated sodium channel, calcium channel and potassium channels, and some second massager coupled channels. For neural functions of the central nervous system, synaptic transmission is the main procedure for which information is transmitted between neurons through brain regions, and intact synaptic function is fundamentally important for almost all the nervous functions, including consciousness, memory, and cognition. Therefore, it is important to understand the effects of general anesthetics on synaptic transmission via modulations of specific ion channels and relevant molecular targets, which can lead to the development of safer general anesthetics with selective actions. The present review will summarize the effects of various general anesthetics on synaptic transmissions and plasticity.
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Kerssens, Chantal, Takashi Ouchi, and Peter S. Sebel. "No Evidence of Memory Function during Anesthesia with Propofol or Isoflurane with Close Control of Hypnotic State." Anesthesiology 102, no. 1 (2005): 57–62. http://dx.doi.org/10.1097/00000542-200501000-00012.
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Background The authors previously demonstrated memory function during apparently adequate general anesthesia in trauma patients. Hypnotic state fluctuations, stress, and variable amnesic qualities of commonly used anesthetics could account for this effect. Methods The authors replicated the trauma investigation in 90 elective surgical patients to enable anesthetic titration to a bispectral index value of 50-55 during auditory presentation of word stimuli. Patients were randomly assigned to maintenance with propofol (n = 48) or isoflurane (n = 42). Before surgery, state anxiety and trait anxiety were assessed using self-report measures. Postoperative memory assessment relied on the process dissociation procedure using a word stem completion task. Results There were no differences between groups for relevant demographic, preoperative, or supplemental drug variables. Ninety-eight percent of words were presented within a bispectral index range of 40-60, with values averaging 48.8 (SD = 5.7) during word presentation. Neither the process dissociation procedure nor standard measures of conscious recall and recognition memory showed evidence of explicit or implicit memory. Preoperative stress levels did not correlate with postoperative memory test scores in either study group. Conclusions In contrast to the results of their previous study, the authors found no evidence of memory function with close control of hypnotic state. This suggests that hypnotic state fluctuations are important to memory activation under anesthesia. Other variables may contribute to preserved memory function as well. Propofol and isoflurane block memory equally well during adequate anesthesia.
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Zhu, Changlian, Jianfeng Gao, Niklas Karlsson, et al. "Isoflurane Anesthesia Induced Persistent, Progressive Memory Impairment, Caused a Loss of Neural Stem Cells, and Reduced Neurogenesis in Young, but Not Adult, Rodents." Journal of Cerebral Blood Flow & Metabolism 30, no. 5 (2010): 1017–30. http://dx.doi.org/10.1038/jcbfm.2009.274.
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Isoflurane and related anesthetics are widely used to anesthetize children, ranging from premature babies to adolescents. Concerns have been raised about the safety of these anesthetics in pediatric patients, particularly regarding possible negative effects on cognition. The purpose of this study was to investigate the effects of repeated isoflurane exposure of juvenile and mature animals on cognition and neurogenesis. Postnatal day 14 (P14) rats and mice, as well as adult (P60) rats, were anesthetized with isoflurane for 35 mins daily for four successive days. Object recognition, place learning and reversal learning as well as cell death and cytogenesis were evaluated. Object recognition and reversal learning were significantly impaired in isoflurane-treated young rats and mice, whereas adult animals were unaffected, and these deficits became more pronounced as the animals grew older. The memory deficit was paralleled by a decrease in the hippocampal stem cell pool and persistently reduced neurogenesis, subsequently causing a reduction in the number of dentate gyrus granule cell neurons in isoflurane-treated rats. There were no signs of increased cell death of progenitors or neurons in the hippocampus. These findings show a previously unknown mechanism of neurotoxicity, causing cognitive deficits in a clearly age-dependent manner.
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Bagabas, Ahmed M., Mootaaz M. Ashi, Ahmed O. Alamoudi, Sameer A. Alaidarous, Sohaib K. Filemban, and Wadeeah K. Bahaziq. "Knowledge about anesthesia and the role of anesthesiologists among Jeddah citizens." International Journal of Research in Medical Sciences 5, no. 6 (2017): 2779. http://dx.doi.org/10.18203/2320-6012.ijrms20172486.
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Background: The anesthesiologist has a vital role in the operating theatres. Awareness of the role of the anesthesiologist and the types of anesthesia is essential for every person. This study was made to estimate how much information the general population have about the anesthesiologist and the different types of anesthesia.Methods: This research was a cross sectional non-interventional study. The research team conducted a questionnaire in which each participant in the study was interviewed by the research team. The sample size was 159 participants.Results: From the participants,99 (62.2%) recognized the anesthesiologist as a specialized doctor who administers the anesthetics,62 (38.9%) know that the anesthesiologist has a role in resuscitating the patient with the team if crises occurred. However, 85 (53.4%) believe that the surgeon has the responsibility of postoperative pain management. Physicians were the source of knowledge for most participant’s information.Conclusions: A reasonable percentage of people appreciated the role of the anesthesiologist in administrating the anesthesia, however there is a lack of information about the role of the anesthesiologist intra and postoperatively. The need for more education for people about anesthesia is essential as the amount of information about anesthesia in general is rather low.
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Badenes, Rafael, Ega Qeva, Giovanni Giordano, Nekane Romero-García, and Federico Bilotta. "Intranasal Insulin Administration to Prevent Delayed Neurocognitive Recovery and Postoperative Neurocognitive Disorder: A Narrative Review." International Journal of Environmental Research and Public Health 18, no. 5 (2021): 2681. http://dx.doi.org/10.3390/ijerph18052681.
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Delayed neurocognitive recovery and postoperative neurocognitive disorders are major complications of surgery, hospitalization, and anesthesia that are receiving increasing attention. Their incidence is reported to be 10–80% after cardiac surgery and 10–26% after non-cardiac surgery. Some of the risk factors include advanced age, level of education, history of diabetes mellitus, malnutrition, perioperative hyperglycemia, depth of anesthesia, blood pressure fluctuation during surgery, chronic respiratory diseases, etc. Scientific evidence suggests a causal association between anesthesia and delayed neurocognitive recovery or postoperative neurocognitive disorders, and various pathophysiological mechanisms have been proposed: mitochondrial dysfunction, neuroinflammation, increase in tau protein phosphorylation, accumulation of amyloid-β protein, etc. Insulin receptors in the central nervous system have a non-metabolic role and act through a neuromodulator-like action, while an interaction between anesthetics and central nervous system insulin receptors might contribute to anesthesia-induced delayed neurocognitive recovery or postoperative neurocognitive disorders. Acute or chronic intranasal insulin administration, which has no influence on the blood glucose concentration, appears to improve working memory, verbal fluency, attention, recognition of objects, etc., in animal models, cognitively healthy humans, and memory-impaired patients by restoring the insulin receptor signaling pathway, attenuating anesthesia-induced tau protein hyperphosphorylation, etc. The aim of this review is to report preclinical and clinical evidence of the implication of intranasal insulin for preventing changes in the brain molecular pattern and/or neurobehavioral impairment, which influence anesthesia-induced delayed neurocognitive recovery or postoperative neurocognitive disorders.
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Kodama, Mitsuyoshi, Yasushi Satoh, Yukiko Otsubo, et al. "Neonatal Desflurane Exposure Induces More Robust Neuroapoptosis than Do Isoflurane and Sevoflurane and Impairs Working Memory." Anesthesiology 115, no. 5 (2011): 979–91. http://dx.doi.org/10.1097/aln.0b013e318234228b.
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Background In animal models, neonatal exposure to volatile anesthetics induces neuroapoptosis, leading to memory deficits in adulthood. However, effects of neonatal exposure to desflurane are largely unknown. Methods Six-day-old C57BL/6 mice were exposed to equivalent doses of desflurane, sevoflurane, or isoflurane for 3 or 6 h. Minimum alveolar concentration was determined by the tail-clamp method as a function of anesthesia duration. Apoptosis was evaluated by immunohistochemical staining for activated caspase-3, and by TUNEL. Western blot analysis for cleaved poly-(adenosine diphosphate-ribose) polymerase was performed to examine apoptosis comparatively. The open-field, elevated plus-maze, Y-maze, and fear conditioning tests were performed to evaluate general activity, anxiety-related behavior, working memory, and long-term memory, respectively. Results Minimum alveolar concentrations at 1 h were determined to be 11.5% for desflurane, 3.8% for sevoflurane, and 2.7% for isoflurane in 6-day-old mice. Neonatal exposure to desflurane (8%) induced neuroapoptosis with an anatomic pattern similar to that of sevoflurane or isoflurane; however, desflurane induced significantly greater levels of neuroapoptosis than almost equivalent doses of sevoflurane (3%) or isoflurane (2%). In adulthood, mice treated with these anesthetics had impaired long-term memory, whereas no significant anomalies were detected in the open-field and the elevated plus-maze tests. Although performance in a working memory task was normal in mice exposed neonatally to sevoflurane or isoflurane, mice exposed to desflurane had significantly impaired working memory. Conclusions In an animal model, neonatal desflurane exposure induced more neuroapoptosis than did sevoflurane or isoflurane and impaired working memory, suggesting that desflurane is more neurotoxic than sevoflurane or isoflurane.
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Ibrahim, Andra E., Mohamed M. Ghoneim, Evan D. Kharasch, et al. "Speed of Recovery and Side-effect Profile of Sevoflurane Sedation Compared with Midazolam." Anesthesiology 94, no. 1 (2001): 87–94. http://dx.doi.org/10.1097/00000542-200101000-00018.
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Background Sedation for surgical procedures performed with regional or local anesthesia has usually been achieved with intravenous medications, whereas the use of volatile anesthetics has been limited. The use of sevoflurane for sedation has been suggested because of its characteristics of nonpungency, rapid induction, and quick elimination. The purpose of this investigation was to assess the quality, recovery, and side effects of sevoflurane sedation compared with midazolam. Methods One hundred seventy-three patients undergoing surgery with local or regional anesthesia were enrolled in a multicenter, open-label, randomized investigation comparing sedation with sevoflurane versus midazolam. Sedation level was titrated to an Observer's Assessment of Alertness--Sedation score of 3 (responds slowly to voice). Recovery was assessed objectively by Observer's Assessment of Alertness--Sedation, Digit Symbol Substitution Test (DSST), and memory scores, and subjectively by visual analog scales. Results Significantly more patients in the sevoflurane group had to be converted to general anesthesia because of excessive movement (18 sevoflurane and 2 midazolam; P = 0.043). Of remaining patients, 141 were assessable for efficacy and recovery data (93 sevoflurane and 48 midazolam). Sevoflurane and midazolam produced dose-related sedation. Sevoflurane patients had higher DSST and memory scores during recovery. Seventy-six percent (sevoflurane) compared with 35% (midazolam) returned to baseline DSST at 30 min postoperatively (P < 0.05). More frequent excitement-disinhibition was observed with sevoflurane (15 [16%] vs. midazolam; P = 0.008). Conclusions Sevoflurane for sedation produces faster recovery of cognitive function as measured by DSST and memory scores compared with midazolam. However, sevoflurane for sedation is complicated by a high incidence of intraoperative excitement.
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Semba, Kazunori, Naoto Adachi, and Tatsuru Arai. "Facilitation of Serotonergic Activity and Amnesia in Rats Caused by Intravenous Anesthetics." Anesthesiology 102, no. 3 (2005): 616–23. http://dx.doi.org/10.1097/00000542-200503000-00021.
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Background Midazolam and propofol often provoke retrograde amnesia after recovery from anesthesia in humans. Because an increase in central serotonergic activity impairs learning and memory, the authors examined the relation between changes in the serotonergic activity caused by intravenous anesthetics and memory. Methods Changes in extracellular concentrations of monoamines and their metabolites were investigated in rat striatum by a microdialysis procedure, and the effects of intraperitoneal injections of midazolam (5 mg/kg), propofol (60 mg/kg), and pentobarbital (15 mg/kg) were then examined. To evaluate the behavioral alteration with these agents, the authors used a step-through passive avoidance test. Results Midazolam and propofol slightly increased the extracellular concentration of 5-hydroxytryptamine in the striatum, although pentobarbital did not produce any changes. Midazolam and propofol increased the extracellular concentration of 5-hydroxyindoleacetic acid, a metabolite of 5-hydroxytryptamine, with the peak values each 138% and 138% of that in saline-injected animals, respectively. However, pentobarbital decreased the 5-hydroxyindoleacetic acid concentration to 61% of that in the saline group. Administration of midazolam or propofol immediately after the completing the passive avoidance learning reduced step-through latencies after 24 h, although pentobarbital-injected animals maintained a consistent performance. The effects of midazolam and propofol on step-through latencies were completely antagonized by intracerebroventricular administration of spiroxatrine (5 microg), a 5-hydroxytryptamine 1A antagonist, 30 min before training. Conclusions Midazolam and propofol increased central serotonergic activity and provoked retrograde amnesia. Because amnesia was completely diminished by a 5-hydroxytryptamine antagonist, facilitation of the serotonergic system may be involved in retrograde amnesia caused by these agents.
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Cascella, Marco. "Anesthesia awareness. Can midazolam attenuate or prevent memory consolidation on intraoperative awakening during general anesthesia without increasing the risk of postoperative delirium?" Korean Journal of Anesthesiology 68, no. 2 (2015): 200. http://dx.doi.org/10.4097/kjae.2015.68.2.200.
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Zolotareva, L. S., O. N. Paponov, S. M. Stepanenko, A. V. Adler, E. S. Feduleeva, and E. V. Silina. "Prevention of cognitive disorders in the postoperative period in preschoolers." Voprosy praktičeskoj pediatrii 15, no. 4 (2020): 92–99. http://dx.doi.org/10.20953/1817-7646-2020-4-92-99.
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Surgeries under general anesthesia may result in reduced cognitive functions in children, which is important for child development Objective. To assess the incidence of cognitive disorders in children aged 3 to 7 years after intraoperative combined balanced anesthesia and to evaluate the efficacy of Cytoflavin in preventing them. Patients and methods. This study included 85 children who had undergone surgery (adenoidectomy and/or tonsillectomy) under general combined balanced anesthesia (sevoflurane, nitrous oxide, rocuronium bromide, fentanyl, and dexamethasone). The patients were randomized into two groups: control group (n = 40) and experimental group, in which children additionally received one infusion of cytoflavin intraoperatively (n = 44). All patients underwent comprehensive testing with the assessment of various cognitive functions before surgery, 24 hours postoperatively, and one month postoperatively. Results. Cognitive disorders were observed in 6%–10% of children after general anesthesia. The main manifestations of cognitive deficits in the postoperative period, such as impaired concentration, were most significant 24 hours postoperatively, but were eliminated one month later. A total of 7.1% of children demonstrated at least 20% decrease of their attention after surgery under general balanced anesthesia (confirmed by at least 3 tests). Six percent of children had a 20% decrease in their memory 24 hours postoperatively (confirmed by 2 tests). Cytoflavin improved cognitive performance 24 hours postoperatively, while patients in the control group had no significant changes. However, administration of cytoflavin had no significant impact on the incidence of cognitive deficit. Further studies are needed to identify children at risk who require prevention of cognitive disorders associated with anesthesia. Key words: anesthesia in children, anesthetics, pediatric surgery, cognitive outcomes, nicotinamide, postoperative cognitive dysfunction, cytoflavin
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Tao, Guorong, Qingsheng Xue, Yan Luo, Guohui Li, Yimeng Xia та Buwei Yu. "Isoflurane Is More Deleterious to Developing Brain Than Desflurane: The Role of the Akt/GSK3βSignaling Pathway". BioMed Research International 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/7919640.
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Demand is increasing for safer inhalational anesthetics for use in pediatric anesthesia. In this regard, researchers have debated whether isoflurane is more toxic to the developing brain than desflurane. In the present study, we compared the effects of postnatal exposure to isoflurane with those of desflurane on long-term cognitive performance and investigated the role of the Akt/GSK3βsignaling pathway. Postnatal day 6 (P6) mice were exposed to either isoflurane or desflurane, after which the phosphorylation levels of Akt/GSK3βand learning and memory were assessed at P8 or P31. The phosphorylation levels of Akt/GSK3βand learning and memory were examined after intervention with lithium. We found that isoflurane, but not desflurane, impaired spatial learning and memory at P31. Accompanied by behavioral change, only isoflurane decreased p-Akt (ser473) and p-GSK3β(ser9) expressions, which led to GSK3βoveractivation. Lithium prevented GSK3βoveractivation and alleviated isoflurane-induced cognitive deficits. These results suggest that isoflurane is more likely to induce developmental neurotoxicity than desflurane in context of multiple exposures and that the Akt/GSK3βsignaling pathway partly participates in this process. GSK3βinhibition might be an effective way to protect against developmental neurotoxicity.
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Hadžimešić, Munevera, Semir Imamović, Vasvija Uljić, Mirsad Hodžić, Fatima Iljazagić-Halilović, and Renata Hodžić. "Cognitive function recovery rate in early postoperative period: comparison of propofol, sevoflurane and isoflurane anesthesia." Journal of Health Sciences 3, no. 1 (2013): 48–54. http://dx.doi.org/10.17532/jhsci.2013.29.
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Introduction: There is no simple answer to the question as to when the brain function is back to normal after anaesthesia. Research done so far has identified different factors influencing the rate of cognitive function recovery and type of anaesthetic as one of those factors.Methods: This study encountered 90 patients hospitalized in neurosurgical department of University Clinical Centre Tuzla in period from October 2011 to may 2012 year. Aim of the study was to compare influence of three different anesthetics (propofol, isofl urane and sevofl urane) on recovery rate of cognitive performance 1, 5 and 10 minutes following extubation. Assessment of cognitive functions was preformed using the short Orientation-Memory-Concentration (OMC) Test. All patients included in the study underwent lumbar microdiscectomy surgery and were allocated to one of three groups: propofol, sevoflurane and isoflurane.Results: Trough comparison of OMC test values there is obvious superiority in recovery of cognitive functions between propofol group and inhaled anesthetic group, after 1 minute (p = 0.008) and after 5 minutes (p =0.009). Comparison of propofol and isoflurane anesthesia shows significantly faster recovery of cognitive performance in propofol group (after 1 minute p = 0.002, 5 minutes p = 0.004, 10 minutes p = 0.038). Faster recovery of cognitive function is present in sevoflurane compared to isoflurane group only 1 minute after extubation p = 0.049.Conclusions: Fastest recovery of cognitive performance appears after propofol anesthesia, than follows sevofl urane based anesthesia and after that isoflurane anesthesia.
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Saab, Bechara J., Ashley J. B. MacLean, Marijana Kanisek та ін. "Short-term Memory Impairment after Isoflurane in Mice Is Prevented by the α5 γ-Aminobutyric Acid Type A Receptor Inverse Agonist L-655,708". Anesthesiology 113, № 5 (2010): 1061–71. http://dx.doi.org/10.1097/aln.0b013e3181f56228.
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Background Memory blockade is an essential component of the anesthetic state. However, postanesthesia memory deficits represent an undesirable and poorly understood adverse effect. Inhibitory α5 subunit-containing γ-aminobutyric acid subtype A receptors (α5GABAA) are known to play a critical role in memory processes and are highly sensitive to positive modulation by anesthetics. We postulated that inhibiting the activity of α5GABAA receptors during isoflurane anesthesia would prevent memory deficits in the early postanesthesia period. Methods Mice were pretreated with L-655,708, an α5GABAA receptor-selective inverse agonist, or vehicle. They were then exposed to isoflurane for 1 h (1.3%, or 1 minimum alveolar concentration, or air-oxygen control). Then, either 1 or 24 h later, mice were conditioned in fear-associated contextual and cued learning paradigms. In addition, the effect of L-655,708 on the immobilizing dose of isoflurane was studied. Motor coordination, sedation, anxiety, and the concentration of isoflurane in the brain at 5 min, 1 h, and 24 h after isoflurane were also examined. Results Motor and sensory function recovered within minutes after termination of isoflurane administration. In contrast, a robust deficit in contextual fear memory persisted for at least 24 h. The α5GABAA receptor inverse agonist, L-655,708, completely prevented memory deficits without changing the immobilizing dose of isoflurane. Trace concentrations of isoflurane were measured in the brain 24 h after treatment. Conclusions Memory deficits occurred long after the sedative, analgesic, and anxiolytic effects of isoflurane subsided. L-655,708 prevented memory deficit, suggesting that an isoflurane interaction at α5GABAA receptors contributes to memory impairment during the early postanesthesia period.
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Sanchez, Victoria, Shawn D. Feinstein, Nadia Lunardi, et al. "General Anesthesia Causes Long-term Impairment of Mitochondrial Morphogenesis and Synaptic Transmission in Developing Rat Brain." Anesthesiology 115, no. 5 (2011): 992–1002. http://dx.doi.org/10.1097/aln.0b013e3182303a63.
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Background Clinically used general anesthetics, alone or in combination, are damaging to the developing mammalian brain. In addition to causing widespread apoptotic neurodegeneration in vulnerable brain regions, exposure to general anesthesia at the peak of synaptogenesis causes learning and memory deficiencies later in life. In vivo rodent studies have suggested that activation of the intrinsic (mitochondria-dependent) apoptotic pathway is the earliest warning sign of neuronal damage, suggesting that a disturbance in mitochondrial integrity and function could be the earliest triggering events. Methods Because proper and timely mitochondrial morphogenesis is critical for brain development, the authors examined the long-term effects of a commonly used anesthesia combination (isoflurane, nitrous oxide, and midazolam) on the regional distribution, ultrastructural properties, and electron transport chain function of mitochondria, as well as synaptic neurotransmission, in the subiculum of rat pups. Results This anesthesia, administered at the peak of synaptogenesis, causes protracted injury to mitochondria, including significant enlargement of mitochondria (more than 30%, P < 0.05), impairment of their structural integrity, an approximately 28% increase in their complex IV activity (P < 0.05), and a twofold decrease in their regional distribution in presynaptic neuronal profiles (P < 0.05), where their presence is important for the normal development and functioning of synapses. Consequently, the authors showed that impaired mitochondrial morphogenesis is accompanied by heightened autophagic activity, decrease in mitochondrial density (approximately 27%, P < 0.05), and long-lasting disturbances in inhibitory synaptic neurotransmission. The interrelation of these phenomena remains to be established. Conclusion Developing mitochondria are exquisitely vulnerable to general anesthesia and may be important early target of anesthesia-induced developmental neurodegeneration.
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Wang, Quan, Jingcong Luo, Ruiqiang Sun та Jia Liu. "MicroRNA-1297 suppressed the Akt/GSK3β signaling pathway and stimulated neural apoptosis in an in vivo sevoflurane exposure model". Journal of International Medical Research 49, № 4 (2021): 030006052098210. http://dx.doi.org/10.1177/0300060520982104.
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Objective Common inhalation anesthetics used for clinical anesthesia (such as sevoflurane) may induce nerve cell apoptosis during central nervous system development. Furthermore, anesthetics can produce cognitive impairments, such as learning and memory impairments, that continue into adulthood. However, the precise mechanism remains largely undefined. We aimed to determine the function of microRNA-1297 (miR-1297) in sevoflurane-induced neurotoxicity. Methods Reverse transcription-polymerase chain reaction assays were used to analyze miR-1297 expression in sevoflurane-exposed mice. MTT and lactate dehydrogenase (LDH) assays were used to measure cell growth, and neuronal apoptosis was analyzed using flow cytometry. Western blot analyses were used to measure PTEN, PI3K, Akt, and GSK3β protein expression. Results In sevoflurane-exposed mice, miR-1297 expression was up-regulated compared with the control group. MiR-1297 up-regulation led to neuronal apoptosis, inhibition of cell proliferation, and increased LDH activity in the in vitro model of sevoflurane exposure. MiR-1297 up-regulation also suppressed the Akt/GSK3β signaling pathway and induced PTEN protein expression in the in vitro model. PTEN inhibition (VO-Ohpic trihydrate) reduced PTEN protein expression and decreased the effects of miR-1297 down-regulation on neuronal apoptosis in the in vitro model. Conclusion Collectively, the results indicated that miR-1297 stimulates sevoflurane-induced neurotoxicity via the Akt/GSK3β signaling pathway by regulating PTEN expression.
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Schaefer, Michele L., Meina Wang, Patric J. Perez, Wescley Coca Peralta, Jing Xu, and Roger A. Johns. "Nitric Oxide Donor Prevents Neonatal Isoflurane-induced Impairments in Synaptic Plasticity and Memory." Anesthesiology 130, no. 2 (2019): 247–62. http://dx.doi.org/10.1097/aln.0000000000002529.
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Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background In humans, multiple early exposures to procedures requiring anesthesia constitute a significant risk factor for development of learning disabilities and disorders of attention. In animal studies, newborns exposed to anesthetics develop long-term deficits in cognition. Previously, our laboratory showed that postsynaptic density (PSD)-95, discs large homolog, and zona occludens-1 (PDZ) domains may serve as a molecular target for inhaled anesthetics. This study investigated a role for PDZ interactions in spine development, plasticity, and memory as a potential mechanism for early anesthetic exposure-produced cognitive impairment. Methods Postnatal day 7 mice were exposed to 1.5% isoflurane for 4 h or injected with 8 mg/kg active PSD-95 PDZ2WT peptide. Apoptosis, hippocampal dendritic spine changes, synapse density, long-term potentiation, and cognition functions were evaluated (n = 4 to 18). Results Exposure of postnatal day 7 mice to isoflurane or PSD-95 PDZ2WT peptide causes a reduction in long thin spines (median, interquartile range [IQR]: wild type control [0.54, 0.52 to 0.86] vs. wild type isoflurane [0.31, 0.16 to 0.38], P = 0.034 and PDZ2MUT [0.86, 0.67 to 1.0] vs. PDZ2WT [0.55, 0.53 to 0.59], P = 0.028), impairment in long-term potentiation (median, IQR: wild type control [123, 119 to 147] and wild type isoflurane [101, 96 to 118], P = 0.049 and PDZ2MUT [125, 119 to 131] and PDZ2WT [104, 97 to 107], P = 0.029), and deficits in acute object recognition (median, IQR: wild type control [79, 72 to 88] vs. wild type isoflurane [63, 55 to 72], P = 0.044 and PDZ2MUT [81, 69 to 84] vs. PDZ2WT [67, 57 to 77], P = 0.039) at postnatal day 21 without inducing detectable differences in apoptosis or changes in synaptic density. Impairments in recognition memory and long-term potentiation were preventable by introduction of a NO donor. Conclusions Early disruption of PDZ domain–mediated protein–protein interactions alters spine morphology, synaptic function, and memory. These results support a role for PDZ interactions in early anesthetic exposure–produced cognitive impairment. Prevention of recognition memory and long-term potentiation deficits with a NO donor supports a role for the N-methyl-d-aspartate receptor/PSD-95/neuronal NO synthase pathway in mediating these aspects of isoflurane-induced cognitive impairment.
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Schaefer, Michele L., Patric J. Perez, Meina Wang, et al. "Neonatal Isoflurane Anesthesia or Disruption of Postsynaptic Density-95 Protein Interactions Change Dendritic Spine Densities and Cognitive Function in Juvenile Mice." Anesthesiology 133, no. 4 (2020): 812–23. http://dx.doi.org/10.1097/aln.0000000000003482.
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Background Experimental evidence shows postnatal exposure to anesthesia negatively affects brain development. The PDZ2 domain, mediating protein–protein interactions of the postsynaptic density-95 protein, serves as a molecular target for several inhaled anesthetics. The authors hypothesized that early postnatal disruption of postsynaptic density-95 PDZ2 domain interactions has persistent effects on dendritic spines and cognitive function. Methods One-week-old mice were exposed to 1.5% isoflurane for 4 h or injected with 8 mg/kg active postsynaptic density-95 wild-type PDZ2 peptide along with their respective controls. A subset of these mice also received 4 mg/kg of the nitric oxide donor molsidomine. Hippocampal spine density, long-term potentiation, novel object recognition memory, and fear learning and memory were evaluated in mice. Results Exposure of 7-day-old mice to isoflurane or postsynaptic density-95 wild-type PDZ2 peptide relative to controls causes: (1) a long-term decrease in mushroom spines at 7 weeks (mean ± SD [spines per micrometer]): control (0.8 ± 0.2) versus isoflurane (0.4 ± 0.2), P < 0.0001, and PDZ2MUT (0.7 ± 0.2) versus PDZ2WT (0.4 ± 0.2), P < 0.001; (2) deficits in object recognition at 6 weeks (mean ± SD [recognition index]): naïve (70 ± 8) versus isoflurane (55 ± 14), P = 0.010, and control (65 ± 13) versus isoflurane (55 ± 14), P = 0.045, and PDZ2MUT (64 ±11) versus PDZ2WT (53 ± 18), P = 0.045; and (3) deficits in fear learning at 7 weeks and memory at 8 weeks (mean ± SD [% freezing duration]): Learning, control (69 ± 12) versus isoflurane (52 ± 13), P < 0.0001, and PDZ2MUT (65 ± 14) versus PDZ2WT (55 ± 14) P = 0.011, and Memory, control (80 ± 17) versus isoflurane (56 ± 23), P < 0.0001 and PDZ2MUT (73 ± 18) versus PDZ2WT (44 ± 19) P < 0.0001. Impairment in long-term potentiation has fully recovered here at 7 weeks (mean ± SD [% baseline]): control (140 ± 3) versus isoflurane (137 ± 8), P = 0.560, and PDZ2MUT (136 ± 17) versus PDZ2WT (128 ± 11), P = 0.512. The isoflurane induced decrease in mushroom spines was preventable by introduction of a nitric oxide donor. Conclusions Early disruption of PDZ2 domain-mediated protein–protein interactions mimics isoflurane in decreasing mushroom spine density and causing learning and memory deficits in mice. Prevention of the decrease in mushroom spine density with a nitric oxide donor supports a role for neuronal nitric oxide synthase pathway in mediating this cellular change associated with cognitive impairment. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New
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Lazar, Ronald M., Randolph S. Marshall, J. P. Mohr, William L. Young, and John Pile-Spellman. "Unanticipated memory loss during superselective Wada testing for right cerebral arteriovenous malformation." Stroke 32, suppl_1 (2001): 337–38. http://dx.doi.org/10.1161/str.32.suppl_1.337-d.
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120 Background: A major concern in the treatment of cerebral AVMs is whether so-called eloquent regions occupy normal anatomic locations. Recently, we have shown with selective anesthetic injections that language has a wide and unusual distribution in patients with left cerebral AVM. Our Objective here was to determine whether superselective Wada testing in medial right-hemisphere arteries would produce verbal memory loss in patients with right cerebral AVM. Methods: Nine patients, 8 right- and 1 left-handed, had superselective injections of amobarbital sodium plus lidocaine into vessels near or feeding right medial AVMs. Five patients had AVMs supplied by PCA feeders and four had ACA feeders. Memory testing occurred in a no-anesthetic baseline, 1 minute after anesthetic injection, and 12 minutes after injection. A memory test consisted of 5 words presented on a computer screen which the patient had to read aloud. After 3 minutes, recall was tested. A maximum score was 15, with uncued recall of a word = 3 points, prompted recall = 2 points, and multiple choice = 1 point. Based on clinical considerations, various numbers of vessels were tested in each patient. Results: Superselective anesthetic testing in most vessels yielded memory scores no different than baseline, and embolization took place. In each patient, however, there was at least one vessel feeding the AVM in which significant short-term verbal memory loss took place. In these instances, the mean memory score at baseline was 14 (s.d. = 1.5). Following injection of anesthetics, the mean score fell significantly to 7.1 (t-test, p<.00001). Attention was unaltered. After dissipation of the anesthesia at 12 minutes, memory returned to baseline levels in every case. Conclusions: In nine patients, superselective Wada injection into arteries feeding right medial AVMs produced unanticipated verbal memory deficits. Traditional assumptions about eloquent regions would have suggested that such testing would have been unnecessary, but embolization here would have yielded significant morbidity. Our findings also question established notions of verbal memory restricted to the left hemisphere.
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Brinker, Andrea, Kate Prior, and Jan Schumacher. "Personal Protection during Resuscitation of Casualties Contaminated with Chemical or Biological Warfare Agents—A Survey of Medical First Receivers." Prehospital and Disaster Medicine 24, no. 6 (2009): 525–28. http://dx.doi.org/10.1017/s1049023x00007457.
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AbstractIntroduction:The threat of mass casualties caused by an unconventional terrorist attack is a challenge for the public health system, with special implications for emergency medicine, anesthesia, and intensive care. Advanced life support of patients injured by chemical or biological warfare agents requires an adequate level of personal protection. The aim of this study was to evaluate the personal protection knowledge of emergency physicians and anesthetists who would be at the frontline of the initial health response to a chemical/biological warfare agent incident.Methods:After institutional review board approval, knowledge of personal protection measures among emergency medicine (n = 28) and anesthetics (n = 47) specialty registrars in the South Thames Region of the United Kingdom was surveyed using a standardized questionnaire. Participants were asked for the recommended level of personal protection if a chemical/biological warfare agent(s) casualty required advanced life support in the designated hospital resuscitation area.Results:The best awareness within both groups was regarding severe acute respiratory syndrome, and fair knowledge was found regarding anthrax, plague, Ebola, and smallpox. In both groups, knowledge about personal protection requirements against chemical warfare agents was limited. Knowledge about personal protection measures for biological agents was acceptable, but was limited for chemical warfare agents.Conclusions:The results highlight the need to improve training and education regarding personal protection measures for medical first receivers.
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Cattano, Davide, Nicholas C. Lam, Lara Ferrario, et al. "Dexmedetomidine versus Remifentanil for Sedation during Awake Fiberoptic Intubation." Anesthesiology Research and Practice 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/753107.
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This study compared remifentanil and dexmedetomidine as awake fiberoptic intubation (AFOI) anesthetics. Thirty-four adult ASA I-III patients were enrolled in a double-blinded randomized pilot study to receive remifentanil (REM) or dexmedetomidine (DEX) for sedation during AFOI (nasal and oral). Thirty patients completed the study and received 2 mg midazolam IV and topical anesthesia. The REM group received a loading dose of 0.75 mcg/kg followed by an infusion of 0.075 mcg/kg/min. The DEX group received a loading dose of 0.4 mcg/kg followed by an infusion of 0.7 mcg/kg/hr. Time to sedation, number of intubation attempts, Ramsay sedation scale (RSS) score, bispectral index (BIS), and memory recall were recorded. All thirty patients were successfully intubated by AFOI (22 oral intubations/8 nasal). First attempt success rate with AFOI was higher in the REM group than the DEX group, 72% and 38% (P=0.02), respectively. The DEX group took longer to attain RSS of ≥3 and to achieve BIS <80, as compared to the REM group. Postloading dose verbal recall was poorer in the DEX group. Dexmedetomidine seems a useful adjunct for patients undergoing AFOI but is dependent on dosage and time. Further studies in the use of dexmedetomidine for AFOI are warranted.
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Song, Ruixue, Xiaomin Ling, Mengyuan Peng, Zhanggang Xue, Jing Cang, and Fang Fang. "Maternal Sevoflurane Exposure Causes Abnormal Development of Fetal Prefrontal Cortex and Induces Cognitive Dysfunction in Offspring." Stem Cells International 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/6158468.
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Maternal sevoflurane exposure during pregnancy is associated with increased risk for behavioral deficits in offspring. Several studies indicated that neurogenesis abnormality may be responsible for the sevoflurane-induced neurotoxicity, but the concrete impact of sevoflurane on fetal brain development remains poorly understood. We aimed to investigate whether maternal sevoflurane exposure caused learning and memory impairment in offspring through inducing abnormal development of the fetal prefrontal cortex (PFC). Pregnant mice at gestational day 15.5 received 2.5% sevoflurane for 6 h. Learning function of the offspring was evaluated with the Morris water maze test at postnatal day 30. Brain tissues of fetal mice were subjected to immunofluorescence staining to assess differentiation, proliferation, and cell cycle dynamics of the fetal PFC. We found that maternal sevoflurane anesthesia impaired learning ability in offspring through inhibiting deep-layer immature neuron output and neuronal progenitor replication. With the assessment of cell cycle dynamics, we established that these effects were mediated through cell cycle arrest in neural progenitors. Our research has provided insights into the cell cycle-related mechanisms by which maternal sevoflurane exposure can induce neurodevelopmental abnormalities and learning dysfunction and appeals people to consider the neurotoxicity of anesthetics when considering the benefits and risks of nonobstetric surgical procedures.
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Satomoto, Maiko, Yasushi Satoh, Katsuo Terui, et al. "Neonatal Exposure to Sevoflurane Induces Abnormal Social Behaviors and Deficits in Fear Conditioning in Mice." Anesthesiology 110, no. 3 (2009): 628–37. http://dx.doi.org/10.1097/aln.0b013e3181974fa2.
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Background Neonatal exposure to anesthetics that block N-methyl-D-aspartate receptors and/or hyperactivate gamma-aminobutyric acid type A receptor has been shown to cause neuronal degeneration in the developing brain, leading to functional deficits later in adulthood. The authors investigated whether exposure of neonatal mice to inhaled sevoflurane causes deficits in social behavior as well as learning disabilities. Methods Six-day-old C57BL/6 mice were exposed to 3% sevoflurane for 6 h. Activated cleaved caspase-3 immunohistochemical staining was used for detection of apoptosis. Cognitive functions were tested by pavlovian conditioned fear test. Social behavior was tested by social recognition and interaction tests. Results Neonatal exposure to sevoflurane significantly increased the number of apoptotic cells in the brain immediately after anesthesia. It caused persistent learning deficits later in adulthood as evidenced by decreased freezing response in both contextual and cued fear conditioning. The social recognition test demonstrated that mice with neonatal exposure to sevoflurane did not develop social memory. Furthermore, these mice showed decreased interactions with a social target compared with controls in the social interaction test, indicating a social interaction deficit. The authors did not attribute these abnormalities in social behavior to impairments of general interest in novelty or olfactory sensation, because they did not detect significant differences in the test for novel inanimate object interaction or for olfaction. Conclusions This study shows that exposure of neonatal mice to inhaled sevoflurane could cause not only learning deficits but also abnormal social behaviors resembling autism spectrum disorder.
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Wang, Jin, Xinyi Li, Huisheng Wu, Jianjuan Ke, Zongze Zhang, and Yanlin Wang. "Effects of L-655,708 on expression changes of GABA, glutamate, and beta-endorphin induced by propofol anesthesia in rats." European Journal of Inflammation 16 (January 2018): 205873921879670. http://dx.doi.org/10.1177/2058739218796708.
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Anesthetics are considered to be one of the important inducing factors of postoperative cognitive dysfunction (POCD). The hippocampal region of the rat is one of the action sites of general anesthesia drugs. L 655,708, a reverse agonist of gamma aminobutyric acid (GABA) receptor, can significantly improve short-term memory dysfunction in mice after anesthetized with isoflurane. So the purpose of this study is to investigate the effects of L-655,708 on expression of GABA, glutamate (GLU), and beta-endorphin (β-EP) in the dentate gyrus region of the hippocampus and cognition of rats anesthetized with propofol. In all, 30 male Sprague–Dawley (SD) rats were randomly allocated into the control group, sham group, and L-655,708 group, with 10 in each group. The cognitive function of rats was measured by Morris water maze before and 1 h after administration. Then the rats were sacrificed for brain tissues. Immunohistochemistry was used to study the expression of GABA, GLU, and β-EP in the hippocampus of anesthetized rats in each group. Compared with the control group, the latency of the sham group and L-655,708 group were significantly prolonged after administration ( P < 0.05). However, L-655,708 could shorten the prolonged latency ( P < 0.05). There was no significant difference in times of accessing original platform area between the three groups before and after medication ( P > 0.05). The expression level of GABA in the dentate gyrus region of hippocampus of rats in the sham group was significantly higher than that in the control group ( P < 0.05), while the expression level in the L-655,708 group was significantly lower than that in the sham group ( P < 0.05). No significant difference was found in the expression of GLU in the dentate gyrus region of hippocampus of rats in each group ( P > 0.05). Compared with the control group, the expression of β-EP was significantly lower in the dentate gyrus region of the hippocampus of sham group rats ( P < 0.05). However, the expression of β-EP in the L-655,708 group was significantly higher than that in the sham group ( P < 0.05). Cognitive dysfunction in rats anesthetized with propofol may be related to high expression of GABA and low expression of β-EP in the hippocampus. The mechanism of L-655,708 in reducing the cognitive impairment in propofol anesthetized rats may be bound up with down-regulating the expression of GABA and increasing the expression of β-EP in the hippocampus.
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Dorofeeva, G. S. "The influence of the chosen method of anesthesia on the severity of postoperative cognitive dysfunction in patients with ophthalmic surgery." Medicni perspektivi (Medical perspectives) 26, no. 1 (2021): 122–28. http://dx.doi.org/10.26641/2307-0404.2021.1.227948.
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Reduction of cognitive functions in the postoperative period is gaining importance in the context of the insurance medicine introduction. Operational stress and anaesthetization are factors which increase the risk of deepening and developing postoperative cognitive dysfunction. The function of short-term memory, attention function, and the speed of psychomotor cognitive reactions are the most vulnerable to the action of general anesthetics. The influence of various methods of anesthesia on cognitive functions in ophthalmic surgery patients after end-to-end keratoplasty has been studied in this research work. Dexmedetomidine was used (the selective agonist of α-adrenoreceptors) as one of the components of multimodal anaesthetization. The sedative effect of this drug is explained by inhibition of neural activity in the blue spot of the brain stem. Dexmedetomidine is known to be used for sedation of patients. It allowed possibility to reduce the amount of fentanyl which was necessary for intra-and post-operative anaesthetization. Our research was conducted on the basis of ME "DRCOH". 78 patients at the age of 18 to 60 years were examined after end-to-end keratoplasty. Non-inclusion criteria: presence of concomitant pathology, neurological diseases, use of psychotropic substances and alcohol 6 months before the study. The study was conducted using neuropsychological testing: the Mini Mental State Examination (MMSE),the Frontal Assessment Battery (FAB), and Luria’s test. Testing was performed before the operation, in 6, 24 hours, 7 and 21 days. Patients were randomized into two groups. The first group – group k (n1=45) included patients who were provided with anaesthetic management according to the following scheme:premedication — ondansetron 4 mg, dexamethasone 4 mg, ketorolac 30 mg intravenously, sibazone 10 mg, fentanyl 0.1 mg intramuscularly 40 minutes before intervention. Induction of propofol – 2-2.5 mg/kg fractionally to achieve clinical symptoms of anaesthetization, fentanyl – 0.005% 0.1 mg tracheal intubation after relaxation on the background of atracuriumbenzylate – 0.3-0.6 mg/kg. Maintaining of anaesthetization: oxygen-sevoflurane mixture FiO250-55%, sevoflurane 1,4-1,8 vol.% on exhalation (1-1. 5 WT.) with the flow of no more than 1 l/min. BIS indicators were kept at the level of 30-40, during the surgery, the bolus injection of 0.1 mg of fentanyl was used in the event of hemodynamic reactions. Anaesthetic support was performed using the infusion of dexmedetomidin for 40 minutes, ondansetron 4 mg, dexamethasone 4 mg, ketorolac 30 mg intravenously in the second group d (n2=33). Induction, relaxation and maintenance of anaesthetization were performed as in the previous group. Intra-operative monitoring of patients in both groups included: non-invasive measurement of blood pressure (BP), heart rate (HR), pulse oximetry, determination of blood gases (oxygen, carbon dioxide and inhaled anesthetic on inhalation and exhalation). Control of the depth of anaesthetization was performed on the basis of BIS and ANI - monitoring. The use of dexmedetomidinu as the component of a multi-modal method of anaesthetizational al lowed obtaining less pronounced POCD, due to the reduction in the number of used drugs. Further use of the combination of highly selective agonists of α2-adrenoreceptors with regional anaesthetization in ophthalmic surgery is the promising method.
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Nader, Nader D. "Ketamine: An Update on Cellular and Subcellular Mechanisms with Implications for Clinical Practice." Pain Physician 2, no. 20;2 (2017): E285—E301. http://dx.doi.org/10.36076/ppj.2017.e301.
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Background: Ketamine is one of the oldest hypnotic agents used to provide an anesthetic agent with analgesic properties and minimal suppressive effects on respiration. The ability of ketamine in modulating glutamatergic (N-methyl D-aspartate) pain receptors has made this anesthetic drug a new option for the management of patients with chronic pain syndromes. Further preclinical and clinical findings suggest ketamine may have wide ranging effects on both cognition and development. Recent advances have revealed an unprecedented role for ketamine in the acute management of depression. Objectives: The purpose of this review is to integrate a number of basic science, preclinical, and clinical studies with the goal of providing insight into the possible signaling events underlying ketamine’s biological effects in pain management, depression, cognition and memory, and neurodevelopment. Study Design: Narrative literature review. Setting: Health science library. Methods: A comprehensive literature search was performed for the following medical subject headings and keywords (ketamine, anesthesia, pain, analgesia, depression, NMDA receptors) on PubMed, Google Scholar, and Medline from 1966 to the present time. The search was then limited to those in the English language. The full text of the relevant articles were printed and reviewed by all authors. Results: We provided a comprehensive review of the literature that explored the pharmacologic aspects of ketamine from its conception as an anesthetic to its evolution as a drug used for treatment of depression and pain. To address the patient response variability observed in clinical studies, we have provided possible patient-specific factors that could contribute to outcome variability. Limitations: Like any review, this study was limited by publication bias and missing information on negative studies which were denied publication. Conclusions: Ketamine, an old anesthetic agent with analgesic properties, is currently being considered for treating patients with chronic pain and depression. The complex pharmacological characteristics of ketamine make this medication a multifaceted therapeutic option in these cases. Key Words: Ketamine, anesthetics, pain, depression, pharmacology
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Zhong, Yushuang, and Ravi Prakash. "Subconscious Auditory Processing in Anesthesia: The Common Theme Between Dreams, Implicit Memory and Anesthesia Awareness." NeuroQuantology 12, no. 4 (2014). http://dx.doi.org/10.14704/nq.2014.12.4.752.
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"The 9th International Symposium on Memory and Awareness in Anesthesia (MAA9)." British Journal of Anaesthesia 115 (July 2015): i122—i144. http://dx.doi.org/10.1093/bja/aev204.
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"The importance of maintaining normal perioperative physiological parameters in children during anaesthesia." Signa Vitae, 2021. http://dx.doi.org/10.22514/sv.2021.058.
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Every year, millions of neonates, infants and young children need general anesthesia for a variety of procedures. As pediatric anesthesia remains at high risk of perioperative morbidity and mortality, attention has been directed towards the anesthesia training and the anesthetics safety. We are now reassured about the relatively safeness of the anesthetic drugs, but the safest intraoperative conduct has still to be determined. In the absence of clear evidence, it appears logical to prevent perturbations of the child “baseline”, by avoiding preoperative distress, maintaining normal intraoperative parameters and preventing postoperative discomfort. Recently, ten “N” principles (no fear/awareness, normovolemia, normotension, normal heart rate, normoxemia, normocapnia, normonatremia, normoglycemia, normotermia and no pain/nausea/vomiting/emergence delirium) have been proposed as the base of a safer anesthesia care. The current paper aims to summarize the current evidence behind the “10-Ns” rational and to help guide anesthesiologists in their practice.
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Platholi, Jimcy, and Hugh C. Hemmings Jr. "Effects of general anesthetics on synaptic transmission and plasticity." Current Neuropharmacology 19 (August 3, 2021). http://dx.doi.org/10.2174/1570159x19666210803105232.
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: General anesthetics depress excitatory and/or enhance inhibitory synaptic transmission principally by modulating the function of glutamatergic or GABAergic synapses, respectively, with relative anesthetic agent-specific mechanisms. Synaptic signaling proteins, including ligand- and voltage-gated ion channels, are targeted by general anesthetics to modulate various synaptic mechanisms including presynaptic neurotransmitter release, postsynaptic receptor signaling, and dendritic spine dynamics to produce their characteristic acute neurophysiological effects. As synaptic structure and plasticity mediate higher-order functions such as learning and memory, long-term synaptic dysfunction following anesthesia may lead to undesirable neurocognitive consequences depending on specific anesthetic agent and the vulnerability of population. Here we review the cellular and molecular mechanisms of transient and persistent general anesthetic alterations of synaptic transmission and plasticity.
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Zhao, Shuai, Ziqi Fan, Jing Hu, et al. "The differential effects of isoflurane and sevoflurane on neonatal mice." Scientific Reports 10, no. 1 (2020). http://dx.doi.org/10.1038/s41598-020-76147-6.
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Abstract Previous research has shown that exposure to volatile anesthetics can induce acute neuroinflammation and neuroapoptopsis in neonatal rodents and that these events can lead to cognitive dysfunction at later stages. Isoflurane and sevoflurane are two of the most popular anesthetics used in the field of pediatrics. However, the relative impact of these two anesthetics on the developing brain at distinct time points after the induction of anesthesia has not been compared. In the present study, we exposed 7-day-old mice to clinically equivalent doses of isoflurane (1.5%) and sevoflurane (2.5%) for 4 h and then investigated consequential changes in the brains of these mice at six different time points. We analyzed the levels of proteins that are directly related to neuroapoptosis, neuroinflammation, synaptic function, and memory, in the brains of neonatal mice. Exposure of neonatal mice to isoflurane and sevoflurane resulted in acute neuronal apoptosis. Our analysis observed significant levels of neuroinflammation and changes in the expression levels of proteins associated with both synaptic transmission and memory in mice from the isoflurane group but not the sevoflurane group. Our results therefore indicate that isoflurane and sevoflurane induce differential effects in the brains of neonatal mice.
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Saito, Kota, Sho Ohno, Makishi Maeda, Naoyuki Hirata, and Michiaki Yamakage. "Remimazolam anesthesia for cardiac surgery with cardiopulmonary bypass: a case report." JA Clinical Reports 7, no. 1 (2021). http://dx.doi.org/10.1186/s40981-021-00424-0.
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Abstract Background Remimazolam has less cardiovascular depressant effects than propofol in non-cardiac surgical patients. However, the efficacy and safety of remimazolam in cardiac surgery with cardiopulmonary bypass (CPB) have not been reported. We present a case of successful anesthetic management using remimazolam in cardiac surgery with CPB. Case presentation A 76-year-old female was scheduled for mitral valve repair, tricuspid annuloplasty, maze procedure, and left atrial appendage closure. We used remimazolam in induction (6.0 mg/kg/h) and maintenance (0.6–1.0 mg/kg/h) of general anesthesia, and the bispectral index value was maintained in the range of 36 to 48 including the period of CPB. Hemodynamics, mixed venous oxygen saturation, and bilateral regional cerebral oxygen saturation were maintained within acceptable ranges. There was no intraoperative awareness/recall or serious complications associated with remimazolam throughout the perioperative period. Conclusions Remimazolam can be used the same as other existing anesthetics in cardiac surgery with CPB.
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Leung, L. Stan, and Tao Luo. "Cholinergic Modulation of General Anesthesia." Current Neuropharmacology 19 (April 21, 2021). http://dx.doi.org/10.2174/1570159x19666210421095504.
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: Acetylcholine in the brain serves arousal and cognitive functions. Cholinergic neurons in the mesopontine brainstem and basal forebrain are important for activation of the cerebral cortex, which is characterized by suppression of irregular slow waves and increase in gamma (30-100 Hz) activity in the electroencephalogram, and appearance of a hippocampal theta rhythm. During general anesthesia, decrease in acetylcholine release and cholinergic functions contribute to the desirable outcomes of general anesthesia such as amnesia, loss of awareness and consciousness, and immobility. Animal experiments indicate that inactivation, lesion or genetic ablation of cholinergic neurons in the basal forebrain potentiated the effects of inhalational and injectable anesthetics, including isoflurane, halothane, propofol, pentobarbital and in some cases, ketamine. Increased behavioral sensitivity to general anesthetic, faster induction time and delayed recovery of a loss of righting reflex have been shown in rodents with basal forebrain cholinergic deficits. Cholinergic stimulation in the prefrontal cortex, thalamus and basal forebrain hastens recovery from general anesthesia. Anticholinesterase accelerates emergence from general anesthesia, but with mixed success, in part depending on the anesthetic used. Cholinergic deficits may contribute to cognitive impairments after anesthesia and operations, which are severe in aged subjects. We propose a cholinergic hypothesis for postoperative cognitive disorder, in line with the cholinergic deficits and cognitive decline in aging and Alzheimer’s disease. The current animal literature suggests that brain cholinergic neurons can regulate the immune and inflammatory response after surgical operation and anesthetic exposure, and anticholinesterase and α7-nicotinic cholinergic agonists can alleviate postoperative inflammatory response and cognitive deficits.