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Emergence delirium (ED) is a common neurologic complication that can not only distress children and their families in the early postanesthetic period, but can also have adverse effects on children in the long-term. This study aimed to investigate the effects of single-dose dexmedetomidine on ED in children with sevoflurane anesthesia and to observe postoperative behavioral changes through long-term follow-up. Patients aged 2-7 years, American Society of Anesthesiologists class (ASA) I or II, scheduled for tonsillectomy with and without adenoidectomy were randomized to receive dexmedetomidine 0.5 μg/kg (Group D) or volume-matched normal saline (Group C) over 10 minutes after induction of anesthesia. The primary outcome was the incidence of ED within 30 minutes after extubation. Other outcomes were the incidence of pain, extubation time, post-anesthesia care unit (PACU) length of stay after extubation, adverse events, and the incidence of negative postoperative behavioral changes (NPOBCs). Ninety children completed the study. Compared with the control group (Group C), dexmedetomidine decreased the incidence of ED (31.1% vs 53.3%; =0.033) and pain (28.9% vs 57.8%; =0.006), but it prolonged extubation time ( ⩽0.001). PACU length of stay after extubation and the percentage of adverse events were similar between groups. The incidence of NPOBCs in Group D was significantly lower at 1 and 7 days after discharge (33.3% vs 60.0%; =0.011% and 24.4% vs 46.7%; =0.028, respectively) than it was in Group C, but no significant difference was found at the 30th day. Dexmedetomidine 0.5 μg/kg reduced the incidence of ED after sevoflurane anesthesia and might be used to prevent NPOBCs. ChiCTR1800016828.

There is scarce evidence on the hemodynamic stability of remimazolam during anesthetic induction in patients with significant coronary artery disease. This study aims to compare the effects of remimazolam and propofol on post-induction hypotension in patients undergoing coronary artery bypass grafting (CABG). Randomized controlled trial. Tertiary teaching hospital. Adult patients undergoing isolated CABG. Patients were randomly allocated to received either remimazolam (n = 50) or propofol (n = 50) for anesthetic induction. The remimazolam group received an initial infusion at 6 mg/kg/h, which was later adjusted to 1–2 mg/kg/h to maintain a bispectral index of 40–60 after loss of consciousness. In the propofol group, a 1.5 mg/kg bolus of propofol was administered, followed by 1–1.5% sevoflurane inhalation as needed to achieve the target bispectral index. The primary outcome was the area under the curve (AUC) below the baseline mean arterial pressure (MAP) during the first 10 min after anesthetic induction. Secondary outcomes included the AUC for MAP <65 mmHg and the requirement for vasopressors. The remimazolam group demonstrated a significantly lower AUC under the baseline MAP compared to the propofol group (mean [SD], 169.8 [101.0] mmHg·min vs. 220.6 [102.4] mmHg·min; mean difference [95% confidence interval], 50.8 [10.4–91.2] mmHg·min; P = 0.014). Additionally, the remimazolam group had a reduced AUC for MAP <65 mmHg (7.3 [10.3] mmHg·min vs. 13.9 [14.9] mmHg·min; P = 0.007) and a lower frequency of vasopressor use compared to the propofol group (60% vs. 88%, P = 0.001). Remimazolam may offer improved hemodynamic stability during anesthetic induction in patients undergoing CABG, suggesting its potential advantage over propofol for patients with significant coronary artery disease in terms of hemodynamic stability. [Display omitted] •Remimazolam reduced MAP decrease during anesthesia induction by 23% than propofol.•Remimazolam use needed less vasopressors and kept higher MAP levels than propofol.•Remimazolam offers better hemodynamic stability for anesthesia induction for CABG.

Lipid metabolism has been considered as a potential therapeutic target in sevoflurane‐induced neurotoxicity that can potentially affect the learning and memory function in the developmental brain. Recently, triggering receptor expressed on myeloid cells 2 (TREM2) is identified as a crucial step in regulating lipid metabolism and associated with the pathogenesis of neurodegenerative diseases. Herein, it is reported that quercetin modified Cu2‐xSe (abbreviated as CSPQ) nanoparticles can ameliorate sevoflurane‐induced neurotoxicity by tuning the microglial lipid metabolism and promoting microglial M2‐like polarization via TREM2 signaling pathway, in which the apolipoprotein E (ApoE), and adenosine triphosphate‐binding cassette transporters (ABCA1 and ABCG1) levels are upregulated. Furthermore, the protective effects of CSPQ nanoparticles against sevoflurane‐induced neurotoxicity via TREM2 are further demonstrated by the small interfering RNA (siRNA)‐TREM2 transfected BV2 cells, which are obviously not influenced by CSPQ nanoparticles. The cell membrane coated CSPQ (referred as CSPQ@CM) nanoparticles can significantly reduce sevoflurane‐induced learning and memory deficits, improve lipid metabolism dysfunction, and promote the remyelination in the hippocampus of mice. The study shows great potential of targeting microglial lipid metabolism in promoting remyelination of neurons for treatment of neurotoxicity and neurodegenerative diseases. Lipid droplets as the components of myelin sheath and neuron cell membranes play an important role in the brain. Sevoflurane exposures in the neonatal can lead to developmental neurotoxicity through dysmyelination. Quercetin functionalized Cu2‐xSe nanoparticles are used to modulate the lipid metabolism and polarization of microglia to improve the sevoflurane induced‐developmental neurotoxicity by targeting the surface TREM2.

Background Perioperative neurocognitive disorders (PND) with a high incidence frequently occur in elderly surgical patients closely associated with prolonged anesthesia-induced neurotoxicity. The neuromorphopathological underpinnings of anesthesia-induced neurotoxicity have remained elusive. Methods Prolonged anesthesia with sevoflurane was used to establish the sevoflurane-induced neurotoxicity (SIN) animal model. Morris water maze, elevated plus maze, and open field test were employed to track SIN rats’ cognitive behavior and anxiety-like behaviors. We investigated the neuropathological basis of SIN through techniques such as transcriptomic, electrophysiology, molecular biology, scanning electron microscope, Golgi staining, TUNEL assay, and morphological analysis. Our work further clarifies the pathological mechanism of SIN by depleting microglia, inhibiting neuroinflammation, and C1q neutralization. Results This study shows that prolonged anesthesia triggers activation of the NF-κB inflammatory pathway, neuroinflammation, inhibition of neuronal excitability, cognitive dysfunction, and anxiety-like behaviors. RNA sequencing found that genes of different types of synapses were downregulated after prolonged anesthesia. Microglial migration, activation, and phagocytosis were enhanced. Microglial morphological alterations were also observed. C1qa, the initiator of the complement cascade, and C3 were increased, and C1qa tagging synapses were also elevated. Then, we found that the “Eat Me” complement pathway mediated microglial synaptic engulfment in the hippocampus after prolonged anesthesia. Afterward, synapses were remarkably lost in the hippocampus. Furthermore, dendritic spines were reduced, and their genes were also downregulated. Depleting microglia ameliorated the activation of neuroinflammation and complement and rescued synaptic loss, cognitive dysfunction, and anxiety-like behaviors. When neuroinflammatory inhibition or C1q neutralization occurred, complement was also decreased, and synaptic elimination was interrupted. Conclusions These findings illustrated that prolonged anesthesia triggered neuroinflammation and complement-mediated microglial synaptic engulfment that pathologically caused synaptic elimination in SIN. We have demonstrated the neuromorphopathological underpinnings of SIN, which have direct therapeutic relevance for PND patients.

The effects of remote ischemic preconditioning (RIPC) in cardiac surgery have been inconsistent. We investigated whether anesthesia or beta-blockers interfere with RIPC cardioprotection. Fifty patients undergoing cardiac surgery were randomized to receive limb RIPC (four cycles of 5-min of upper arm cuff inflation/deflation) in the awake state (no-anesthesia; n = 17), or under sevoflurane (n = 17) or propofol (n = 16) anesthesia. In a separate crossover study, 11 healthy volunteers received either carvedilol or no medication prior to RIPC. Plasma dialysates were obtained and perfused through an isolated male Sprague–Dawley rat heart subjected to 30-min ischemia/60-min reperfusion, following which myocardial infarct (MI) size was determined. In the cardiac surgery study, pre-RIPC MI sizes were similar among the groups (39.7 ± 4.5% no-anesthesia, 38.9 ± 5.3% sevoflurane, and 38.6 ± 3.6% propofol). However, post-RIPC MI size was reduced in the no-anesthesia group (27.5 ± 8.0%; p < 0.001), but not in the anesthesia groups (35.7 ± 6.9% sevoflurane and 35.8 ± 5.8% propofol). In the healthy volunteer study, there was a reduction in MI size with RIPC in the no-carvedilol group (41.7 ± 4.3% to 30.6 ± 8.5%; p < 0.0001), but not in the carvedilol group (41.0 ± 4.0% to 39.6 ± 5.6%; p = 0.452). We found that the cardioprotective effects of limb RIPC were abolished under propofol or sevoflurane anesthesia and in the presence of carvedilol therapy.

This study investigates the influence of sevoflurane and desflurane on the electrochemical behavior of the Fe(III)-acetylacetonate (Fe(acac)[sub.3]) complex. Using cyclic voltammetry (CV), we demonstrate that while Fe(acac)[sub.3] exhibits reversible redox behavior in an oxygen-free environment, the presence of dissolved oxygen renders the system irreversible, leading to the formation of a thick, reddish film on the electrode surface upon potential cycling. Notably, the addition of sevoflurane and desflurane restores the electrochemical reversibility and dramatically inhibits this film formation. Raman spectroscopy of the resulting films confirmed structural changes which are consistent with this inhibiting action. Furthermore, X-ray photoelectron spectroscopy (XPS) analysis reveals that the iron in the film remains predominantly in the Fe[sup.3+] oxidation state even after prolonged electrochemical reduction cycles. These findings suggest that the anesthetics act by inhibiting the interaction between the Fe(acac)[sub.3] complex and oxygen, likely through a spin–decoherence mechanism. This work highlights the critical role of anesthetics in modifying the electrochemical behavior of metal-oxygen complexes, with potential implications for sensing, electrocatalysis, and bio-oriented systems.

Sleep disturbances are common in older patients following major surgery. Both propofol and sevoflurane are frequently used anesthetics. In this study, we compared the effect of propofol- versus sevoflurane-based anesthesia on postoperative sleep quality in this patient population. A randomized clinical trial. A university hospital. Patients aged 65 to 90 years who were scheduled for elective major abdominal surgery. Enrolled patients were randomized to receive either propofol-based intravenous anesthesia or sevoflurane-based inhalational anesthesia. Primary endpoint was total sleep time monitored by actigraphy on the first postoperative night. Secondary endpoints included plasma orexin-A concentrations at various timepoints from baseline (before anesthesia) until the second postoperative morning. From May 23, 2022 to April 3, 2023, 144 patients (mean age 72.9 years; 58.3 % male) were enrolled and randomly assigned. Total sleep time on the first postoperative night was longer with propofol anesthesia (median 150 min [interquartile range 99 to 200]) than with sevoflurane anesthesia (111 min [80 to 160]; median difference 29 min [95 % CI 4 to 53]; P = 0.025). Plasma orexin-A concentration was lower in the propofol group at 1 h after anesthesia induction (median difference − 31.3 pg/mL [95 % CI −58.1 to −2.2]; P = 0.033) and 6:00 on the first postoperative morning (median difference − 29.8 pg/mL [95 % CI -58.3 to −2.3]; P = 0.036). Among older patients undergoing major abdominal surgery, propofol anesthesia, compared with sevoflurane anesthesia, was associated with a longer total sleep time on the first postoperative night. This difference may be partially attributable to lowered plasma orexin-A level. Trial registration: This randomized trial was approved by Biomedical Research Ethical Committee of Peking University First Hospital (No.2022-155) on April 26, 2022. Chinese Clinical Trial Registry (No. ChiCTR2200060120) URL: https://www.chictr.org.cn/showproj.html?proj=169584, May 19, 2022. •Sleep disturbances are common in older patients after major surgery.•Impact of propofol versus sevoflurane on postoperative sleep remains uncertain.•We found that sleep time on the first night was longer after propofol anesthesia.•Effect of propofol on sleep might be partially related to plasma orexin-A level.

Background. Robot-assisted laparoscopic radical prostatectomy (RLRP) can increase intracranial pressure (ICP) related to a change in position. Increasing ICP may result in various ocular complications, which are rare but serious, such as a corneal abrasion and ischemic optic neuropathy. We performed a prospective observational trial using ultrasonographic measurements to compare optic nerve sheath diameter (ONSD) related to ICP between patients who received either propofol or sevoflurane and underwent RLRP. Methods. Thirty-two male patients scheduled to undergo RLRP were assigned into groups according to the anesthetic agent used (group P: propofol, n = 16; group S: sevoflurane, n = 16). ONSD, end-tidal partial pressure of CO2, and blood pressure were measured 10 min after induction of anesthesia (T0), 30 min (T1), 60 min (T2), and 90 min after changing to the steep Trendelenburg position and introducing a pneumoperitoneum (T3) and 10 min after returning the patient’s position to supine (T4) during surgery. Results. No significant differences were observed in the demographic data of the patients, surgery time, or intraoperative variables, including hemodynamic and respiratory variables, at any of the time points. The mean right ONSDs in the propofol and sevoflurane groups were 37.3 and 40.1 mm at 30 min (p=0.003), respectively. The mean left ONSDs were 38.4 and 40.8 mm at 30 min (p=0.021) after changing to the Trendelenburg position. The ONSDs between the two groups were significantly different during surgery. Conclusions. ONSD increased more in the sevoflurane group than in the propofol group during RLRP. Intravenous anesthetics could alleviate the increase in ICP during RLRP.

Elderly patients undergoing pathophysiological changes necessitate clinical tools for cerebral monitoring. This prospective randomized controlled study aimed to explore how cerebral monitoring using Δo2Hbi, ΔHHbi, and ΔcHbi manifests in elderly patients under either propofol or sevoflurane anesthesia. Single-center, prospective, randomization. A single tertiary hospital (Eunpyeong St. Mary's Hospital, College of Medicine, The Catholic University of Korea). Enrolled 100 patients scheduled for urologic surgery under general anesthesia. Inclusion criteria were (a) age 70–80 years, (b) American Society of Anesthesiologists (ASA) physical status I-II. Patients were double-blind randomized to receive propofol-based or sevoflurane anesthesia. Cerebral oximetry-related parameters were measured at 5, 10, 15, 20, and 30 min in a setting devoid of surgery-related factors. The primary outcome focused on the Δo2Hbi pattern in the left and right sides within the propofol and sevoflurane groups. We analyzed 100 patients, 50 patients in each group. In the propofol group, the left Δo2Hbi decreased from 1.4 (3.7) at 5 min to −0.1 (1.8) at 30 min (P < 0.0001), and the right Δo2Hbi decreased from 2.9 (4.2) at 5 min to −0.06 (2.3) at 30 min (P < 0.0001). In the sevoflurane group, the left Δo2Hbi decreased from 1.1 (3.4) at 5 min to −1.4 (4.4) at 30 min (P < 0.0001), and the right Δo2Hbi decreased from 2.0 (3.2) at 5 min to −1.2 (3.9) at 30 min (P < 0.0001). There were no significant differences between the two groups. ΔHHbi did not exhibit significant changes after an initial decrease at 5 min and showed no significant differences between the two groups. In cerebral oximetry, Δo2Hbi and ΔHHbi could emerge as a valuable approach for discerning changes in the underlying baseline status of the brain in elderly patients during anesthesia. •The monitoring of Δo2Hbi, ΔHHbi, and ΔcHbi in cerebral oximeter could detect alterations in the baseline status of cerebral blood flow and cerebral metabolic rate among elderly patients undergoing anesthesia.•Changes in Δo2Hbi and ΔHHbi could facilitate etiology-based management of cerebral desaturation by explicitly identifying the underlying causes of such desaturation.•The combined use of these modalities has demonstrated a more favorable prognosis compared to employing each independently.