Sevoflurane Anesthesia Research Articles

Intraoperative dexmedetomidine infusion might help to preserve the cognitive function of geriatric patients undergoing arthroscopic shoulder surgery

ABSTRACT Objectives This study tried to evaluate the impact of dexmedetomidine (DXM) infusion provided during sevoflurane (SEV) anesthesia on cognitive function (CF) of elderly patients undergoing elective arthroscopic shoulder surgeries. Patients & Methods A total of 140 patients were randomly allocated into Groups S and D. All patients received SEV (0.5–1 MAC) with placebo or DXM (0.6 µg/kg/h) infusions, respectively. CF was evaluated preoperatively, 48-h, 1-wk, and 2-wk postoperative (PO) using the Montreal Cognitive Assessment Test and Mini-Mental State Examination (MMSE). The study outcome is the frequency and severity of PO cognitive dysfunction (POCD). Results At 48-h PO, the frequency of normal CF and scorings were significantly decreased compared to preoperative findings, but were significantly higher in group D. At 1-wk PO, the frequency of normal CF and scores increased in both groups with significant difference in favor of group D, but differences were significantly lower than in preoperative measures. At 2-wk PO, 79.3% of patients regained their normal CF, with significantly higher frequency and score for group D, and the difference compared to preoperative data was insignificant in group D, but it was significant in group S. At 48-h, scorings were positively related to using DXM but were negatively related to age, obesity, and PO analgesia. Regression analysis defined old age as negative and the use of DXM as positive predictor for high scores. Conclusion SEV anesthesia induced reversible short-term POCD. Coupling of DXM infusion with SEV anesthesia decreased the frequency and scores of POCF and fastened resumption of normal CF.

Complete sevoflurane anesthetic for myringotomy tubes is associated with an increased rate of emergence delirium

Complete sevoflurane anesthetic for myringotomy tubes is associated with an increased rate of emergence delirium

Hippocampal HDAC6 promotes POCD by regulating NLRP3-induced microglia pyroptosis via HSP90/HSP70 in aged mice

BackgroundPostoperative Cognitive Dysfunction (POCD) has attracted increased attention, but its precise mechanism remains to be explored. This study aimed to figure out whether HDAC6 could regulate NLRP3-induced pyroptosis by modulating the functions of HSP70 and HSP90 in microglia to participate in postoperative cognitive dysfunction in aged mice. MethodsAnimal models of postoperative cognitive dysfunction in aged mice were established by splenectomy under sevoflurane anesthesia. Morris water maze was used to examine the cognitive function and motor ability. Sixteen-months-old C57BL/6 male mice were randomly divided into six groups: control group (C group), sham surgery group (SA group), splenectomy group (S group), splenectomy + HDAC6 inhibitor ACY-1215 group (ACY group), splenectomy + HDAC6 inhibitor ACY-1215 + HSP70 inhibitor Apoptozole group (AP group), splenectomy + solvent control group (SC group). The serum and hippocampus of mice were taken after mice were executed. The protein levels of HDAC6, HSP90, HSP70, NLRP3, GSDMD-N, cleaved-Caspase-1 (P20), IL-1β were detected by western blotting. Serum IL-1β, IL-6 and S100β were measured using ELISA assay, and cell localization of HDAC6 was detected by immunofluorescence. In vitro experiments, BV2 cells were used to validate whether this mechanism worked in microglia. The protein levels of HDAC6, HSP90, HSP70, NLRP3, GSDMD-N, P20, IL-1β were detected by western blotting and the content of IL-1β in the supernatant was measured using ELISA assay. The degree of acetylation of HSP90, the interaction of HSP70, HSP90 and NLRP3 were analyzed by coimmunoprecipitation assay. ResultsSplenectomy under sevoflurane anesthesia in aged mice could prolong the escape latency, reduce the number of crossing platforms, increase the expression of HDAC6 and activate the NLRP3 inflammasome to induce pyroptosis in hippocampus microglia. Using ACY-1215 could reduce the activation of NLRP3 inflammasome, the pyroptosis of microglia and the degree of spatial memory impairment. Apoptozole could inhibit the binding of HSP70 to NLRP3, reduce the degradation of NLRP3 and reverse the protective effect of HDAC6 inhibitors. The results acquired in vitro experiments closely resembled those in vivo, LPS stimulation led to the pyroptosis of BV2 microglia cells and the release of IL-1β due to the activation of the NLRP3 inflammasome, ACY-1215 showed the anti-inflammatory effect and Apoptozole exerted the opposite effect. ConclusionsOur findings suggest that hippocampal HDAC6 promotes POCD by regulating NLRP3-induced microglia pyroptosis via HSP90/HSP70 in aged mice.

Retracted: Mechanism of Sevoflurane Anesthesia under Hypothermic Cardiopulmonary Bypass on Postoperative Atrial Fibrillation Rhythm in Patients Undergoing Mitral Valve Replacement.

[This retracts the article DOI: 10.1155/2022/5312897.].

Comparison of effect of inhaled anaesthetic (Sevoflurane) versus intravenous (Propofol) anaesthetic on core and peripheral body temperature during general anaesthesia: A randomised control study

: The fall in core body temperature and peripheral body temperature following the administration of anaesthetic agent has been studied and demonstrated so far, along with the comparison of the same parameters following induction with propofol in contrast to that with sevoflurane. But no study so far, has compared the effects of TCI-propofol based anaesthesia with that of sevoflurane based anaesthesia for induction and maintenance, on core and peripheral body temperature and the gradient of temperature between the agents. The studies conducted so far, has shown more fall in core and peripheral body temperature from their respective baseline values when propofol was used for induction of anaesthesia in comparison to the use of sevoflurane. A total of 60 adults were randomized into two groups of 30 each; Group 1 were induced with TCI- propofol at 8mcg/ml plasma concentration and maintaind with TCI-propofol at 2-3mcg/ml plasma concentration and 66% nitrous oxide and 33% oxygen gas mixture. Group 2 were induced with intravenous thiopentone at 3-5mg/kg body weight and maintained with 1-1.5MAC sevoflurane, 66% nitrous oxide and 33% oxygen gas mixture. Core body temperature was measured inserting the temperature probe into nasophraynx and peripheral temperature was measured with the temperature probe inserted onto thenar eminence of either hand. We observed that both anaesthetic agents have caused similar fall in core temperature. However, peripheral temperature fell more with sevoflurane compared to TCI-propofol. In parallel with these observations, the increase in temperature gradient was higher in magnitude for sevoflurane based anaesthesia. The core temperature was comparable between the groups from their respective baseline values. But, the fall in peripheral temperature was more in sevoflurane group, so was the temperature gradient. Thus, TCI-propofol when used in appropriate plasma concentration for induction and maintenance of anaesthesia causes less hypothermia in contrast to sevoflurane.

Comparison of bolus dose administration of propofol and dexmedetomidine for incidence of emergence delirium in pediatric patients undergoing surgery with general anesthesia: A randomized, double-blind trial

Abstract Background and Aims: Emergence delirium (ED) during the postanesthesia recovery phase presents significant challenges, especially among pediatric patients, with incidence rates spanning from 2% to 80%. This study sought to assess and compare the effectiveness of propofol and dexmedetomidine in addressing ED in pediatric patients undergoing sevoflurane anesthesia. The primary aim was to ascertain the prevalence of ED in both treatment cohorts, while secondary outcomes encompassed postoperative pain, hemodynamic responses, and the occurrence of complications. Material and Methods: Eighty children aged 2–6 years scheduled for short infraumbilical surgeries under general anesthesia were recruited in this trial. Propofol (1 mg/kg) or dexmedetomidine (0.3 μg/kg) was administered 10 min before completion of surgery. The Paediatric Anaesthesia Emergence Delirium scale was employed to evaluate ED every 5 min following extubation, wherein a score exceeding 12 was indicative of ED. Postoperative sedation was assessed using the Ramsay Sedation Scale, while pain levels were determined through the Face, Legs, Activity, Cry, and Consolability (FLACC) score. Any potential complications were closely monitored. Results: The incidence of ED at extubation was 2.50% and 70% in group D and P, respectively, and the trend of lower ED incidence was consistently observed at 5, 10, 15, and 30 min postextubation. The relative risk ratio at extubation was 4.103 (95% confidence interval: 2.49–6.76), highlighting a significant reduction of 4.1 times in the risk of ED when dexmedetomidine was administered. The dexmedetomidine group exhibited a lower incidence of postoperative pain. Conclusion: In comparison to propofol, dexmedetomidine demonstrated superior efficacy in reducing ED and postoperative pain in pediatric patients during general anesthesia, when administered before completion of surgery.

Sustained mitigation of ST-segment elevation in a patient with Brugada syndrome type 1 during sevoflurane and remifentanil anesthesia: a case report

BackgroundDuring general anesthesia, patients with Brugada syndrome are at risk of malignant arrhythmias following worsened ST-segment elevation, potentially leading to sudden cardiac death. The protocol for safe anesthetic management of patients with Brugada syndrome has not yet been established.Case presentationA 63-year-old man, diagnosed with a spontaneous Brugada type 1 pattern, was scheduled for a pleural biopsy using video-assisted thoracoscopic surgery under general anesthesia. We planned general anesthesia using volatile induction and maintenance anesthesia with sevoflurane and remifentanil. We monitored ST-segment morphology and observed sustained mitigation of ST-segment elevation throughout general anesthesia.ConclusionThe present case may indicate that safe anesthetic management of patients with Brugada syndrome depends on whether the anesthetics used can reduce ST-segment elevation.

Local orchestration of distributed functional patterns supporting loss and restoration of consciousness in the primate brain

A central challenge of neuroscience is to elucidate how brain function supports consciousness. Here, we combine the specificity of focal deep brain stimulation with fMRI coverage of the entire cortex, in awake and anaesthetised non-human primates. During propofol, sevoflurane, or ketamine anaesthesia, and subsequent restoration of responsiveness by electrical stimulation of the central thalamus, we investigate how loss of consciousness impacts distributed patterns of structure-function organisation across scales. We report that distributed brain activity under anaesthesia is increasingly constrained by brain structure across scales, coinciding with anaesthetic-induced collapse of multiple dimensions of hierarchical cortical organisation. These distributed signatures are observed across different anaesthetics, and they are reversed by electrical stimulation of the central thalamus, coinciding with recovery of behavioural markers of arousal. No such effects were observed upon stimulating the ventral lateral thalamus, demonstrating specificity. Overall, we identify consistent distributed signatures of consciousness that are orchestrated by specific thalamic nuclei.

Astrocytic phagocytosis in the medial prefrontal cortex jeopardises postoperative memory consolidation in mice.

Memory impairment is one of the main characteristics of postoperative cognitive dysfunction. It remains elusive how postoperative pathological changes of the brain link to the memory impairment. The clinical setting of perioperation was mimicked via partial hepatectomy under sevoflurane anaesthesia together with preoperative restraint stress (Hep-Sev-stress) in mice. Memory changes were assessed with fear conditioning. The medial prefrontal cortex (mPFC)-dorsal hippocampus connectivity was evaluated with injecting neurotracer 28 days before surgery. Astrocytic activation was limited via injecting AAV-GFAP-hM4Di-eGFP into the mPFC. Astrocytic and microglial phagocytosis of synapses were visualised with co-labelling hippocampal neuronal axon terminals with PSD-95 and S100β or Iba1. Neuroinflammation and oxidative stress status were also detected. Hep-Sev-stress impaired the memory consolidation (mean [standard error], 49.91 [2.55]% vs. 35.40 [3.97]% in the contextual memory, p = 0.007; 40.72 [2.78]% vs. 27.77 [2.22]% in cued memory, p = 0.002) and the cued memory retrieval (39.00 [3.08]% vs. 24.11 [2.06]%, p = 0.001) in mice when compared with these in the naïve controls. Hep-Sev-stress damaged the connectivity from the dorsal hippocampus to mPFC but not from the mPFC to the dorsal hippocampus and increased the astrocytic but not microglial phagocytosis of hippocampal neuronal axon terminals in the mPFC. The intervention also induced neuroinflammation and oxidative stress in the dorsal hippocampus and the mPFC in a regional-dependent manner. Limiting astrocyte activation in the mPFC alleviated memory consolidation impairment induced by Hep-Sev-stress. Postoperative memory consolidation was impaired due to astrocytic phagocytosis-induced connectivity injury from the dorsal hippocampus to the medial prefrontal cortex.

Echinatin mitigates sevoflurane-induced neurotoxicity through regulation of ferroptosis and iron homeostasis.

Surgery and anesthesia are vital medical interventions, but concerns over their potential cognitive side effects, particularly with the use of inhalational anesthetics like sevoflurane, have surfaced. This study delves into the neuroprotective potential of Echinatin against sevoflurane-induced neurotoxicity and the underlying mechanisms. Echinatin, a natural compound, has exhibited anti-inflammatory, antioxidant, and anticancer properties. Sevoflurane, while a popular anesthetic, is associated with perioperative neurocognitive disorders (PND) and neurotoxicity. Our investigation began with cellular models, where Echinatin demonstrated a significant reduction in sevoflurane-induced apoptosis. Mechanistically, we identified ferroptosis, a novel form of programmed cell death characterized by iron accumulation and lipid peroxidation, as a key player in sevoflurane-induced neuronal injury. Echinatin notably suppressed ferroptosis in sevoflurane-exposed cells, suggesting a pivotal role in neuroprotection. Expanding our research to a murine model, we observed perturbations in iron homeostasis, inflammatory cytokines, and antioxidants due to sevoflurane exposure. Echinatin treatment effectively restored iron balance, mitigated inflammation, and preserved antioxidant levels in vivo. Behavioral assessments using the Morris water maze further confirmed Echinatin's neuroprotective potential, as it ameliorated sevoflurane-induced spatial learning and memory impairments. In conclusion, our study unveils Echinatin as a promising candidate for mitigating sevoflurane-induced neurotoxicity. Through the regulation of ferroptosis, iron homeostasis, and inflammation, Echinatin demonstrates significant neuroprotection both in vitro and in vivo. These findings illuminate the potential for Echinatin to enhance the safety of surgical procedures involving sevoflurane anesthesia, minimizing the risk of cognitive deficits and neurotoxicity.

Epigenetic Mechanism of SETD1B-mediated Histone Methylation in Cognitive Impairment Induced by Sevoflurane Anesthesia in Neonatal Mice

Sevoflurane (Sev) anesthesia is associated with cognitive deficits and neurotoxicity. This study explores the epigenetic mechanism of SET domain containing 1B (SETD1B) in Sev-induced cognitive impairment in neonatal mice. Neonatal mice (C57BL/6, n = 72) were exposed to 3% Sev for 2 h per day at P6, 7, and 8, and the control neonatal mice were only separated from the mother for 2 h. The mice were divided into groups of 12 individuals, with an equal number of male and female mice in each group. Mice were intraperitoneally injected with adenovirus-packaged SETD1B overexpression vector. Behavioral tests (Morris water maze, open field test, T-maze, novel object recognition, etc.) were performed at P30. Mouse hippocampal neuronal cells were cultured in vitro. SETD1B, C-X-C motif chemokine receptor 4 (CXCR4), NLR family pyrin domain containing 1 (NLRP1), Cleaved Caspase1, and GSDMD-N expressions in hippocampal tissues or cells were determined by quantitative real-time polymerase chain reaction and Western blot. SETD1B and histone H3 lysine 4 methylation (H3K4me1, H3K4me2, and H3K4me3) enrichment on the CXCR4 promoter was analyzed by ChIP. Sev insulted cognitive impairment and diminished SETD1B expression in mouse hippocampal tissues. SETD1B overexpression mitigated cognitive impairment, enhanced H3K4me3 levels in hippocampal tissues, and restrained hippocampal neuronal pyroptosis. SETD1B increased CXCR4 expression by elevating the H3K4me3 level on the CXCR4 promoter, thereby curbing NLRP1/Caspase1-mediated hippocampal neuronal pyroptosis. To conclude, SETD1B enhances CXCR4 expression by elevating the H3K4me3 level on the CXCR4 promoter, thereby suppressing NLRP1/Caspase1-triggered hippocampal neuronal pyroptosis and alleviating Sev-induced cognitive impairment in neonatal mice.

Prelimbic cortical pyramidal neurons to ventral tegmental area projections promotes arousal from sevoflurane anesthesia.

General anesthesia has been used in surgical procedures for approximately 180 years, yet the precise mechanism of anesthetic drugs remains elusive. There is significant anatomical connectivity between the ventral tegmental area (VTA) and the prelimbic cortex (PrL). Projections from VTA dopaminergic neurons (VTADA ) to the PrL play a role in the transition from sevoflurane anesthesia to arousal. It is still uncertain whether the prelimbic cortex pyramidal neuron (PrLPyr ) and its projections to VTA (PrLPyr -VTA) are involved in anesthesia-arousal regulation. We employed chemogenetics and optogenetics to selectively manipulate neuronal activity in the PrLPyr -VTA pathway. Electroencephalography spectra and burst-suppression ratios (BSR) were used to assess the depth of anesthesia. Furthermore, the loss or recovery of the righting reflex was monitored to indicate the induction or emergence time of general anesthesia. To elucidate the receptor mechanisms in the PrLPyr -VTA projection's impact on anesthesia and arousal, we microinjected NMDA receptor antagonists (MK-801) or AMPA receptor antagonists (NBQX) into the VTA. Our findings show that chemogenetic or optogenetic activation of PrLPyr neurons prolonged anesthesia induction and promoted emergence. Additionally, chemogenetic activation of the PrLPyr -VTA neural pathway delayed anesthesia induction and promoted anesthesia emergence. Likewise, optogenetic activation of the PrLPyr -VTA projections extended the induction time and facilitated emergence from sevoflurane anesthesia. Moreover, antagonizing NMDA receptors in the VTA attenuates the delayed anesthesia induction and promotes emergence caused by activating the PrLPyr -VTA projections. This study demonstrates that PrLPyr neurons and their projections to the VTA are involved in facilitating emergence from sevoflurane anesthesia, with the PrLPyr -VTA pathway exerting its effects through the activation of NMDA receptors within the VTA.

SOX5 Attenuates Toxicity in Neural Stem Cells Induced by Sevoflurane Anesthesia via Regulating the PI3K/AKT Pathway

SOX5 Attenuates Toxicity in Neural Stem Cells Induced by Sevoflurane Anesthesia via Regulating the PI3K/AKT Pathway

Application of remimazolam-0.6% sevoflurane anesthesia for flash visual evoked potential monitoring during pituitary adenoma resection: a non-inferiority randomized controlled trial

BackgroundFlash visual evoked potential (FVEP) is a critical method for monitoring intraoperative visual function during neurosurgery. A new benzodiazepine drug called remimazolam has recently been used for general anesthesia. However, the impact of remimazolam on FVEP remains unclear. Therefore, we aimed to investigate how remimazolam, in comparison to propofol, when combined with 0.6% sevoflurane anesthesia, affects the FVEP waveform during pituitary adenoma resection.MethodsOverall, 36 patients undergoing pituitary adenoma resection under general anesthesia were randomly assigned to either the remimazolam group (Group R) or the propofol group (Group P) in a prospective, randomized, controlled, non-inferiority trial. For anesthesia induction, a bolus of 0.2 mg/kg remimazolam or 2 mg/kg propofol was intravenously infused for approximately one minute. The anesthesia was maintained by continuous infusion of either remimazolam (0.7-1.0 mg/kg/h) or propofol (4–6 mg/kg/h), in combination with 0.6% sevoflurane, aimed at sustaining the bispectral index (BIS) within the range of 40–60. The primary outcome was the N75-P100 amplitude of FVEP recorded at approximately 20 min after intubation (T0). 10% of the amplitude at T0 in group P was defined as the non-inferiority margin (δ). Confidence interval testing was used to evaluate the non-inferiority hypothesis. The secondary outcomes covered the P100 latency of FVEP, electroretinogram (ERG) b wave amplitude, demographic characteristics, hemodynamics, and occurrence of adverse events.ResultsThe BIS index during anesthesia was comparable between the groups at the same measured time points (P > 0.05). The N75-P100 amplitude at T0 in group R was 7.64 ± 1.36 µV, while it was 6.96 ± 0.95 µV in group P (P = 0.09), with a mean difference of 0.68 µV (95% CI, -0.11 µV to 1.48 µV). The δ was set at 0.7 and the lower limit of the 95% CI exceeded the -δ. Both remimazolam and propofol had little effect on ERG b-wave amplitudes. At the designated time points, FVEP amplitude and P100 latency displayed no appreciable variation between the two groups (P > 0.05). Furthermore, there were no significant differences in the incidence of adverse events related to anesthesia, needle electrodes, or surgery between the two groups (P > 0.05).ConclusionOur findings suggest that remimazolam-0.6% sevoflurane is non-inferior to propofol-0.6% sevoflurane for general anesthesia, based on the FVEP N75-P100 amplitude. The electrophysiological data obtained in both groups indicate that reproducible and stable FVEP and ERG waveforms can be acquired at set time points. Therefore, for reliable FVEP monitoring, remimazolam-0.6% sevoflurane appears to be a safe and effective protocol in general anesthesia.Trials registrationThis study was registered on chictr.org.cn (ChiCTR2200056803, 17/02/2022).

Effects of Cumulative Duration of Repeated Anesthesia Exposure on Fetal Brain Development in the Ovine Model

(J Clin Anesth. 2023;85:111050) This study examines the impact of repeated and prolonged exposure to sevoflurane anesthesia on fetal neurodevelopment in pregnant sheep. The rationale behind this research lies in the concern over the possible negative effects of long or repeated exposure to anesthesia during pregnancy on fetal brain development, particularly based on findings in animal studies. The experiment involves exposing pregnant sheep to different anesthesia regimens and conducting neurobehavioral assessments of their offspring. It aims to determine whether repeated exposure results in neurodevelopmental impairments. The study follows ethical guidelines designed to align with principles promoting humane animal research.

Neurobehavioral Abnormalities in Offspring of Young Adult Male Rats With a History of Traumatic Brain Injury.

Children of parents with traumatic brain injury (TBI) are more likely to develop psychiatric disorders. This association is usually attributed to TBI-induced changes in parents' personality and families' social environment. We tested the hypothesis that offspring of young adult male rats with TBI develop neurodevelopmental abnormalities in the absence of direct social contact with sires. Male Sprague-Dawley rats (F0 generation) in the TBI group underwent moderate TBI via a midline fluid percussion injury that involved craniectomy under sevoflurane (SEVO) anesthesia for 40 min on post-natal Day 60 (P60), while F0 rats in the control group were placed in a new cage, one per cage, for the equivalent time duration. A subset of F0 rats was sacrificed on P66 to assess acute changes in hypothalamic-pituitary-adrenal (HPA) axis and inflammation markers. The remaining F0 males were mated with naive females on P90 to generate offspring (F1 generation). The F0 males and F1 males and females were sequentially evaluated in the elevated plus maze, for pre-pulse inhibition of acoustic startle, in the Morris water maze, and for resting and stress levels of serum corticosterone starting on ∼P105 (F0) and ∼P60 (F1), followed by tissue collection for further analyses. Acutely, the F0 TBI males had messenger RNA (mRNA) transcripts altered to support an increased hypothalamic and hippocampal Na+-K+-Cl- (Slc12a2) Cl- importer / K+-2Cl- (Slc12a5) Cl- exporter ratio and decreased hippocampal glucocorticoid receptors (Nr3c1), as well as increased serum levels of corticosterone, interleukin-1β (IL-1β), and biomarkers of activated hippocampal microglia and astrocytes. Long-term, F0 TBI rats exhibited increased corticosterone concentrations at rest and under stress, anxiety-like behavior, impaired sensory-motor gating, and impaired spatial memory. These abnormalities were underpinned by reduced mRNA levels of hypothalamic and hippocampal mineralocorticoid receptors (Nr3c2), hippocampal Nr3c1, and hypothalamic brain-derived neurotrophic factor (Bdnf), as well as elevated serum levels of IL-1β, and biomarkers of activated hippocampal microglia and astrocytes. F1 male offspring of TBI sires exhibited abnormalities in all behavioral tests, while their F1 female counterparts had abnormal pre-pulse inhibition responses only. F1 male offspring of TBI sires also had reduced mRNA levels of hippocampal Nr3c1 and Nr3c2, as well as hypothalamic and hippocampal Bdnf, whereas increases in inflammatory markers were more profound in F1 females. These findings suggest that offspring of sires with a history of a moderate TBI that involved craniectomy under SEVO anesthesia for 40 min, develop sex-dependent neurobehavioral abnormalities in the absence of direct social interaction between the sire and the offspring.

Consistency analysis of consciousness index and bispectral index in monitoring the depth of sevoflurane anesthesia in laparoscopic surgery.

The Index of Consciousness (IoC) is a new monitoring index of anesthesia depth reflecting the state of consciousness of the brain independently developed by China. The research on monitoring the depth of anesthesia mainly focuses on propofol, and bispectral index (BIS) is a sensitive and accurate objective index to evaluate the state of consciousness at home and abroad. This study mainly analyzed the effect of IoC on monitoring the depth of sevoflurane anesthesia and the consistency and accuracy with BIS when monitoring sevoflurane maintenance anesthesia. To investigate the monitoring value of the Index of Consciousness (IoC) for the depth of sevoflurane anesthesia in laparoscopic surgery. The study population consisted of 108 patients who experienced elective whole-body anesthesia procedures within the timeframe of April 2020 to June 2023 at our hospital. Throughout the anesthesia process, which encompassed induction and maintenance using inhaled sevoflurane, all patients were diligently monitored for both the Bispectral Index (BIS) and the Index of Consciousness (IoC). We conducted an analysis to assess the correlation between IoC and BIS throughout the anesthesia induction process and from the maintenance phase to the regaining of consciousness. To evaluate the predictive accuracy of IoC and BIS for the onset of unconsciousness during induction and the return of consciousness during emergence, we employed receiver operating characteristic (ROC) curve analysis. The mean difference between BIS and IoC, spanning from the pre-anesthesia induction phase to the completion of propofol induction, was 1.3 (95% Limits of Agreement [-53.4 to 56.0]). Similarly, during the interval from the initiation of sevoflurane inhalation to the point of consciousness restoration, the average difference between BIS and IoC was 0.3 (95% LOA [-10.8 to 11.4]). No statistically significant disparities were observed in the data acquired from the two measurement methodologies during both the anesthesia induction process and the journey from maintenance to the regaining of consciousness (P > 0.05). The outcomes of the ROC curve analysis disclosed that the areas under the curve (AUC) for prognosticating the occurrence of loss of consciousness were 0.967 (95% CI [0.935-0.999]) for BIS and 0.959 (95% CI [0.924-0.993]) for IoC, with optimal threshold values set at 81 (sensitivity: 88.10%, specificity: 92.16%) and 77 (sensitivity: 79.55%, specificity: 95.45%) correspondingly. For the prediction of recovery of consciousness, the AUCs were 0.995 (95% CI [0.987-1.000]) for BIS and 0.963 (95% CI [0.916-1.000]) for IoC, each associated with optimal cutoff values of 76 (sensitivity: 92.86%, specificity: 100.00%) and 72 (sensitivity: 86.36%, specificity: 100.00%) respectively. The monitoring of sevoflurane anesthesia maintenance using IoC demonstrates a level of comparability to BIS, and its alignment with BIS during the maintenance phase of sevoflurane anesthesia is robust. IoC displays promising potential for effectively monitoring the depth of anesthesia.

The effect of sevoflurane exposure on cell-type-specific changes in the prefrontal cortex in young mice.

Sevoflurane, the predominant pediatric anesthetic, has been linked to neurotoxicity in young mice, although the underlying mechanisms remain unclear. This study focuses on investigating the impact of neonatal sevoflurane exposure on cell-type-specific alterations in the prefrontal cortex (PFC) of young mice. Neonatal mice were subjected to either control treatment (60% oxygen balanced with nitrogen) or sevoflurane anesthesia (3% sevoflurane in 60% oxygen balanced with nitrogen) for 2 hours on postnatal days (PNDs) 6, 8, and 10. Behavioral tests and single-nucleus RNA sequencing (snRNA-seq) of the PFC were conducted from PNDs 31 to 37. Mechanistic exploration included clustering analysis, identification of differentially expressed genes (DEGs), enrichment analyses, single-cell trajectory analysis, and genome-wide association studies (GWAS). Sevoflurane anesthesia resulted in sociability and cognition impairments in mice. Novel specific marker genes identified 8 distinct cell types in the PFC. Most DEGs between the control and sevoflurane groups were unique to specific cell types. Re-defining 15 glutamatergic neuron subclusters based on layer identity revealed their altered expression profiles. Notably, sevoflurane disrupted the trajectory from oligodendrocyte precursor cells (OPCs) to oligodendrocytes (OLs). Validation of disease-relevant candidate genes across the main cell types demonstrated their association with social dysfunction and working memory impairment. Behavioral results and snRNA-seq collectively elucidated the cellular atlas in the PFC of young male mice, providing a foundation for further mechanistic studies on developmental neurotoxicity induced by anesthesia.

Melatonin Ameliorates Sevoflurane Anesthesia-Induced Deficits in Learning and Memory of Aged Mice Through Nrf2 Signaling Related Ferroptosis.

Our research aimed at investigating the protective effects in aged mice exposed to sevoflurane anesthesia. To assess learning and memory abilities and exploratory behavior, the novel object recognition (NOR) test, Morris water maze (MWM) test, and open field test were employed. Commercial kits were used to measure levels of malondialdehyde, nicotinamide adenine dinucleotide phosphate oxidase activity, superoxide dismutase activity, catalase activity, and iron. The messenger RNA and protein levels of ferritin heavy chain 1, nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1, and glutathione peroxidase 4 in the hippocampus were detected. Treatment with melatonin significantly ameliorated the decrease in exploration time of novel objects and the discrimination index induced by sevoflurane anesthesia. Melatonin also reduced escape latencies and increased the time spent in the target quadrant in the MWM test. In the open field test, melatonin-treated mice exhibited greater exploratory activity, including longer distances traveled and a higher number of rearing events. Further, melatonin treatment markedly decreased the levels of oxidative stress markers and iron in the hippocampus of aged mice exposed to sevoflurane anesthesia. However, the beneficial effects of melatonin were significantly attenuated following treatment with the Nrf2 inhibitor ML385. Our results suggest that melatonin could alleviate learning and memory impairment induced by sevoflurane anesthesia in aged mice through its antioxidant properties, partially through the Nrf2 pathway.

Analysis Comparing the Recovery of Airway Reflexes and Cognitive Ability After Sevoflurane with Desflurane Anesthesia.

Although sevoflurane and desflurane have nearly identical blood-gas solubilities, current research suggests that airway reflexes recover more quickly with desflurane than sevoflurane; however, cognitive function recovery varies substantially. The current study was piloted to appraise the lengths of time needed to recover from anesthesia following desflurane and sevoflurane anesthesia. A prospective clinical trial was piloted among 70 adult non-obese subjects who underwent elective surgery and were classified I-II by the "American Association of Anesthesiologists (ASA)". Sevoflurane and desflurane were tested among the subjects who were equally distributed. These agents were used in accordance with a normal general anaesthesia procedure. After they were extubated, tests for regaining cognitive function and airway reflexes were carried out, and different time intervals were recorded. The observations were calculated and P < 0.05 was used to conduct the statistical analysis. The average amount of time that passed between the patient's first vocal response and their first successful completion of the swallowing test was analogous between the two groups (T2) with 5.25 ± 3.11 vs 5.01 ± 2.12 in sevoflurane and desflurane, respectively. There was no significant variance at T2. For all the other time intervals of T1, T3, and T4, there was evidence of the significant variance.(P = 0.003; 0.0013; <0.001, respectively). Desflurane causes patients to recover more quickly than sevoflurane does after laparoscopic cholecystectomy under controlled circumstances.