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1.
Sensors (Basel) ; 22(11)2022 Jun 03.
Artigo em Inglês | MEDLINE | ID: mdl-35684885

RESUMO

Monitoring the vital signs of mice is an essential practice during imaging procedures to avoid populational losses and improve image quality. For this purpose, a system based on a set of devices (piezoelectric sensor, optical module and thermistor) able to detect the heart rate, respiratory rate, body temperature and arterial blood oxygen saturation (SpO2) in mice anesthetized with sevoflurane was implemented. Results were validated by comparison with the reported literature on similar anesthetics. A new non-invasive electrocardiogram (ECG) module was developed, and its first results reflect the viability of its integration in the system. The sensors were strategically positioned on mice, and the signals were acquired through a custom-made printed circuit board during imaging procedures with a micro-PET (Positron Emission Tomography). For sevoflurane concentration of 1.5%, the average values obtained were: 388 bpm (beats/minute), 124 rpm (respirations/minute) and 88.9% for the heart rate, respiratory rate and SpO2, respectively. From the ECG information, the value obtained for the heart rate was around 352 bpm for injectable anesthesia. The results compare favorably to the ones established in the literature, proving the reliability of the proposed system. The ECG measurements show its potential for mice heart monitoring during imaging acquisitions and thus for integration into the developed system.


Assuntos
Taxa Respiratória , Sinais Vitais , Animais , Camundongos , Monitorização Fisiológica/métodos , Reprodutibilidade dos Testes , Sevoflurano , Sinais Vitais/fisiologia
2.
Int J Clin Pract ; 2022: 7795004, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35685611

RESUMO

The aim of this randomized control trial is to compare the effect of anesthetic agents on blood levels of parathyroid hormone and ionized calcium. 77 American Society of Anesthesiologists I-II patients who would undergo laparoscopic cholecystectomy were enrolled into this prospective study and randomized into 3 groups with sealed envelope technique as Group S: sevoflurane, Group D: desflurane, and Group TIVA: total intravenous anesthesia. The first blood sample was used to check the baseline blood levels of parathyroid hormone and ionized calcium. In Group S or D, maintenance of anesthesia was being performed with 1 MAC (minimum alveolar concentration) sevoflurane or desflurane, respectively, while in Group TIVA, it was performed with 150 mcg/kg/min propofol and 1 mcg/kg/min remifentanil IV infusions. At the 30th minute of anesthesia and at the 1st hour of end of anesthesia, 2nd and 3rd blood samples, respectively, were used to check the blood levels of PTH and Ca. During perioperative period, hemodynamic parameters were also noted. Blood levels of parathyroid hormone at the 30th min after anesthesia were found to be significantly different between groups (P=0,01). The PTH level at the 30th min after anesthesia was found significantly higher in Group S than that of Groups D and TIVA (P=0.005 and P=0.001, respectively). Blood levels of ionized calcium at 30th min after anesthesia were found significantly different between groups (P=0,048). It was found significantly higher in Group TIVA than that in Group S (P=0.024). Desflurane seems to be the best agent for parathyroidectomy procedures. Future research studies are needed to be conducted to reach out more correct and valuable outcomes.


Assuntos
Anestésicos Intravenosos , Cálcio , Período de Recuperação da Anestesia , Anestésicos Intravenosos/farmacologia , Desflurano , Humanos , Hormônio Paratireóideo , Estudos Prospectivos , Sevoflurano
3.
Int J Mol Sci ; 23(11)2022 Jun 02.
Artigo em Inglês | MEDLINE | ID: mdl-35682930

RESUMO

Perioperative neurocognitive disorders are frequently observed in postoperative patients and previous reports have shown that pre-existing mild cognitive impairment with accumulated neuropathology may be a risk factor. Sevoflurane is a general anesthetic agent which is commonly used in clinical practice. However, the effects of sevoflurane in postoperative subjects are still controversial, as both neurotoxic or neuroprotective effects were reported. The purpose of this study is to investigate the effects of sevoflurane in 3 × Tg mice, a specific animal model with pre-existing Alzheimer's disease neuropathology. 3 × Tg mice and wild-type mice were exposed to 2 h of sevoflurane respectively. Cognitive function, glutamate transporter expression, MAPK kinase pathways, and neuronal apoptosis were accessed on day 7 post-exposure. Our findings indicate that sevoflurane-induced cognitive deterioration in 3 × Tg mice, which was accompanied with the modulation of glutamate transporter, MAPK signaling, and neuronal apoptosis in the cortical and hippocampal regions. Meanwhile, no significant impact was observed in wild-type mice. Our results demonstrated that prolonged inhaled sevoflurane results in the exacerbation of neuronal and cognitive dysfunction which depends on the neuropathology background.


Assuntos
Doença de Alzheimer , Anestésicos Inalatórios , Síndromes Neurotóxicas , Doença de Alzheimer/metabolismo , Sistema X-AG de Transporte de Aminoácidos/metabolismo , Anestésicos Inalatórios/efeitos adversos , Animais , Apoptose , Modelos Animais de Doenças , Hipocampo/metabolismo , Humanos , Camundongos , Síndromes Neurotóxicas/metabolismo , Sevoflurano/efeitos adversos
4.
Pain Physician ; 25(3): 283-291, 2022 05.
Artigo em Inglês | MEDLINE | ID: mdl-35652768

RESUMO

BACKGROUND: Percutaneous nephrolithotomy (PCNL) is the first-line and guideline-recommended treatment for large renal calculi. Multimodal analgesia (MMA) comprising a combination of different analgesics is an increasingly popular method for pain control as it has been shown to reduce postoperative pain and reduce opioid use and the risk of opioid misuse, with a shorter recovery time in various procedures and patient populations. OBJECTIVE: In this study, we tested the hypothesis that MMA with propofol and sevoflurane (PS) can decrease pain intensity during surgery and used IoC2 as a real-time index of the analgesic effect of sevoflurane. STUDY DESIGN: Prospective, single-center, double-blind, randomized controlled clinical trial. SETTING: Xuanwu Hospital of Capital Medical University. METHODS: Patients scheduled for elective percutaneous nephrolithotomy from January 2020 to July 2020 were randomized into 2 groups, standard multimodal analgesia (propofol + sevoflurane group) and control (propofol [P] group). The PS group received propofol 2.5 mg/kg/h along with 1% sevoflurane after induction for 30 minutes during the main anesthetic procedure, and the P group received propofol 5 mg/kg/h by intravenous infusion during the operation. Index of consciousness 2 (IoC2), namely nociception index, intraoperative hemodynamic fluctuation, bispectral index (BIS), electromyography, postanesthesia care unit (PACU) length of stay, visual analog scale (VAS) score, and Aldrete and Steward scores were recorded. RESULTS: A total of 153 patients undergoing PCNL were enrolled. The demographic and clinical characteristics were similar between the 2 groups. IoC2 was reduced in the PS group compared to the P group at T10, T11, T12, T13, T14, and T15 time points, indicating that analgesia was more effective in the former. The BIS of the PS group did not differ significantly from that of the P group except at T12, T13, T14, and T15. PACU length of stay was shorter in the PS group than in the P group (mean [SD]: 54.35 [16.61] vs 47.39 [13.15], P = 0.04). VAS pain scores did not differ significantly between the 2 groups. CONCLUSION: MMA with propofol and sevoflurane provided better analgesia than propofol alone and may be an effective method to reduce stress and the intraoperative nociceptive stimulus response in patients undergoing PCNL, thereby promoting rapid postoperative recovery.


Assuntos
Analgesia , Nefrolitotomia Percutânea , Transtornos Relacionados ao Uso de Opioides , Propofol , Humanos , Dor Pós-Operatória/tratamento farmacológico , Propofol/uso terapêutico , Estudos Prospectivos , Sevoflurano/uso terapêutico
5.
Aging (Albany NY) ; 14(11): 4714-4727, 2022 Jun 06.
Artigo em Inglês | MEDLINE | ID: mdl-35666713

RESUMO

This research aimed to explore the influence of TLR deletion on sevoflurane-induced postoperative cognitive dysfunction in neonatal mice. Herein, WT and TLR3 KO neonatal mice, each with 24, were randomly divided into control group, sevoflurane group, and TLR3-/-+sevoflurane group. The hippocampal neurons of WT, TLR3 KO and RIP3 KO neonatal mice in C group, SEV group, TLR3-/-+SEV group and RIP3-/-+SEV group were extracted for in vitro experiments. The results revealed the degeneration and necrosis of nerve cells in SEV group. Microscopic findings indicated that nerve cells showed shrinkage and nuclear hyperchromatism, along with lessening or even disappearance of nuclei and enlargement of cell spaces, and apoptotic cells in the brain tissues were evidently increased. Compared with SEV group, TLR3-/-+SEV group displayed reductions in these phenomena. Additionally, SEV group showed the reduced SHP2 expression and the increased expressions of proteins associated with TLR signaling pathway and apoptosis. Furthermore, there were no obvious differences in the expressions of such proteins in hippocampal neurons between RIP3-/-+SEV and TLR3-/-+SEV groups. The results confirmed that inhibiting RIP3 phosphorylation and suppressing TLR3 expressions exerted the same influence on the expressions of these proteins in the hippocampus of neonatal mice with sevoflurane-induced cognitive dysfunction. Based on these, it is speculated that TLR3 influences neonatal mice with sevoflurane-induced cognitive dysfunction probably by regulating RIP3 phosphorylation.


Assuntos
Disfunção Cognitiva , Éteres Metílicos , Animais , Animais Recém-Nascidos , Apoptose/genética , Encéfalo/metabolismo , Disfunção Cognitiva/induzido quimicamente , Disfunção Cognitiva/genética , Disfunção Cognitiva/metabolismo , Hipocampo/metabolismo , Éteres Metílicos/efeitos adversos , Éteres Metílicos/metabolismo , Camundongos , Necrose , Sevoflurano/farmacologia , Receptor 3 Toll-Like/genética , Receptor 3 Toll-Like/metabolismo
6.
Acta Biochim Pol ; 69(2): 387-391, 2022 Jun 16.
Artigo em Inglês | MEDLINE | ID: mdl-35709303

RESUMO

BACKGROUND: Perioperative neurocognitive disorders (PND) occur frequently and refer to alterations in cognitive function after surgery, especially in elderly patients. PND is characterized as abnormalities of learning, memory, language, and emotions. Cucurbitacin E has been reported to possess various pharmacological properties, including anticancer, antiviral, and anti-inflammatory effects. In this study, we investigated whether cucurbitacin E could alleviate sevoflurane-induced cognitive dysfunction in rats. METHODS: Sprague-Dawley male rats (~6 weeks old) were randomly assigned to three groups: the control group, the Sevoflurane group, and the Sevoflurane + Cucurbitacin E group. Subsequently, the cognitive dysfunction of the rats was evaluated through the morris water maze test. Hematoxylin and eosin (HE) staining was used to measure the pathological change in brain tissues. Enzyme-linked immunosorbent assay (ELISA) kits were used for determinations of S-100 calcium binding protein B (S-100ß) and neuron-specific enolase (NSE) and cytokine. Cell apoptosis was analyzed by TdT-Mediated Nick-End Labeling (TUNEL) staining. Protein levels were confirmed by Western blotting. RESULTS: Cucurbitacin E relieved brain injury in rats induced by sevoflurane. Cucurbitacin E alleviated sevoflurane-induced S-100ß and NSE levels. Additionally, the Morris water maze task revealed that cucurbitacin E attenuated cognition impairment in sevoflurane-induced rats. Sevoflurane increased levels of IL-6, TNF-α and IL-1ß levels, and decreased the level of IL-10. However, cucurbitacin E exhibited opposite effects on these cytokines, which were induced by sevoflurane. Furthermore, cucurbitacin E inhibited sevoflurane-induced neuron apoptosis and NF-κB pathway in rats. CONCLUSION: These findings indicate that cucurbitacin E can improve sevoflurane-induced cognitive dysfunction in rats by regulating NF-κB pathway, which provided a new strategy for PND treatment.


Assuntos
Disfunção Cognitiva , NF-kappa B , Idoso , Animais , Apoptose , Disfunção Cognitiva/induzido quimicamente , Disfunção Cognitiva/tratamento farmacológico , Disfunção Cognitiva/patologia , Citocinas/metabolismo , Hipocampo , Humanos , Masculino , NF-kappa B/metabolismo , Ratos , Ratos Sprague-Dawley , Subunidade beta da Proteína Ligante de Cálcio S100 , Sevoflurano/efeitos adversos , Transdução de Sinais , Triterpenos
7.
Cell Transplant ; 31: 9636897221104447, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35699095

RESUMO

Recent evidence has indicated that inhalational anesthetics may affect the growth and malignant potential of tumor cells and ultimately influence tumor recurrence after surgery. Sevoflurane, a volatile anesthetic, is used extensively in hepatectomy. However, the effect of sevoflurane on the growth of hepatocellular carcinoma (HCC) cells remains unknown. The aim of this study was to explore the effects of sevoflurane on HCC metastasis and its potential mechanisms in the human HCC cell lines, HepG2 and SMMC7721. HepG2 and SMMC7721 cells were treated with 1.7%, 3.4%, and 5.1 % sevoflurane for 6 h. Cell migration was analyzed using invasion, migration, and scratch assays. Based on previous literature, several microRNAs (miRNAs) were screened to determine regulatory miRNA targets of sevoflurane in HepG2 and SMMC7721 cells; miR-665 was detected as a potential target and overexpressed or inhibited in HepG2 and SMMC7721 cells by a lentiviral system. The p-ERK/MMP pathway was also measured by western blotting. Sevoflurane inhibited the migration and invasion of HCC cells in a dose-dependent manner. It also inhibited miR-665 expression in HCC cells. We further observed that sevoflurane inhibited HCC metastasis via miR-665. Sevoflurane-induced downregulation of miRNA-665 led to phosphorylation of ERK and matrix metalloproteinase (MMP-9) via suppression of SPRED1. These results demonstrated that sevoflurane may inhibit invasion and migration via the p-ERK/MMP-9 signaling pathway in HCC cells.


Assuntos
Carcinoma Hepatocelular , Neoplasias Hepáticas , MicroRNAs , Carcinoma Hepatocelular/tratamento farmacológico , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/metabolismo , Linhagem Celular Tumoral , Movimento Celular/genética , Regulação Neoplásica da Expressão Gênica , Células Hep G2 , Humanos , Neoplasias Hepáticas/tratamento farmacológico , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/metabolismo , Metaloproteinase 9 da Matriz/metabolismo , MicroRNAs/metabolismo , Invasividade Neoplásica/genética , Recidiva Local de Neoplasia/genética , Sevoflurano/farmacologia
8.
Analyst ; 147(11): 2484-2493, 2022 May 30.
Artigo em Inglês | MEDLINE | ID: mdl-35535706

RESUMO

In the operation using sevoflurane as an anesthetic, some patients, especially children, will have agitation symptoms after awakening from anesthesia. The incidence of agitation is about 20%, and current detection methods cannot predict the probability of a patient with agitation. In this paper, a magnetic field enhanced photoelectron ionization (MEPEI) miniature time-of-flight mass spectrometer (TOFMS) was developed for point-of-care detection and verification of the relationship between postoperative agitation symptoms and sevoflurane concentration in exhaled breath. The MEPEI source is water vapor resistant and can directly ionize sevoflurane via capillary sampling and obtain its characteristic ion [C4H3F6O]+ (m/z 181), and the analysis time of exhaled breath is only 60 s. Three standard curves of 0.5-80 ppmv, 80-2000 ppmv and 2000-15 000 ppmv were formulated to quantitatively detect sevoflurane in different scenarios, the coefficient of determination (R2) was higher than 0.9882 and the relative standard deviation (RSD) of signal intensity was only 1.24%. The results indicated that four of the 46 child patients had agitation symptoms. Partial least squares-discriminant analysis (PLS-DA) was performed to analyze the data, and an identification and treatment strategy was established for child patients with agitation symptoms. The new miniature MEPEI-TOFMS was also successfully used to evaluate the concentration of sevoflurane in a medical environment. The real-time monitoring of sevoflurane concentration in exhalation indicates the potential of this method for low-cost and convenient point-of-care (POC) detection and diagnosis of agitation symptoms.


Assuntos
Anestésicos Inalatórios , Éteres Metílicos , Período de Recuperação da Anestesia , Criança , Expiração , Humanos , Sistemas Automatizados de Assistência Junto ao Leito , Sevoflurano
9.
Int Immunopharmacol ; 108: 108869, 2022 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-35605434

RESUMO

BACKGROUND: Sevoflurane anesthesia is deemed as potential therapeutic drug for lipopolysaccharide (LPS)-induced acute lung injury (ALI), but the molecular mechanisms have not been fully delineated. AIM: The present study explored the specific molecular mechanism of sevoflurane regulating autophagy to reduce LPS induced ALI. METHODS: Male C57BL/6J mice and mouse pulmonary microvascular endothelial cells (MPVECs) were treated with LPS to construct ALI models, and the levels of inflammation, apoptosis and autophagy were detected after treatment with sevoflurane. Meanwhile, cells were treated with autophagy inhibitor or AMP-activated protein kinase (AMPK)/unc-51 like autophagy activating kinase 1 (ULK1) pathway inhibitor in vitro to detect their effects on cell survival. RESULTS: Sevoflurane reduced inflammation, recovered cell division so as to suppress cell apoptosis and maintain cell survival, and activated autophagic flux in LPS-induced ALI models in vivo and in vitro. Of note, the suppressing effects of sevoflurane on LPS-induced cell death were abrogated by inhibiting autophagy. Moreover, we evidenced that sevoflurane promoted activation of the AMPK/ULK1 pathway in LPS-induced ALI models. Blockage of this pathway abrogated the promoting effects of sevoflurane on cell autophagy and cell viability in LPS-treated cells. CONCLUSION: Collectively, sevoflurane suppresses apoptosis and inflammation via activating protective autophagy, thereby ameliorating LPS-induced ALI, and the AMPK/ULK1/ PIKFYVE pathway is responsible for the process.


Assuntos
Lesão Pulmonar Aguda , Anestesia , Proteínas Quinases Ativadas por AMP/metabolismo , Lesão Pulmonar Aguda/induzido quimicamente , Lesão Pulmonar Aguda/tratamento farmacológico , Lesão Pulmonar Aguda/metabolismo , Animais , Autofagia , Células Endoteliais/metabolismo , Inflamação , Lipopolissacarídeos/farmacologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Fosfatidilinositol 3-Quinases/metabolismo , Sevoflurano/farmacologia , Sevoflurano/uso terapêutico , Transdução de Sinais
10.
Int Immunopharmacol ; 109: 108800, 2022 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-35550264

RESUMO

Pyroptosis is a type of programmed cell death, and pyroptosis-associated inflammatory response is closely associated with the pathogenesis of acute lung injury (ALI). Sevoflurane, a common clinical anesthetic, has been reported as therapeutic drug for ALI. However, the detailed mechanisms by which sevoflurane ameliorates ALI have not been fully delineated. In this study, we found that sevoflurane phosphorylated and activated the GSK-3ß to suppress LPS-induced pyroptotic cell death, inflammation and ALI. Specifically, in the LPS-induced ALI mice models, sevoflurane attenuated lung damages and fibrosis, and restrained the production of the pro-inflammatory cytokines. Also, LPS increased the expression levels of pyroptosis-related proteins to promote pyroptotic cell death in ALI mice lung tissues, and LPS-induced pyroptotic cell death was reduced by sevoflurane co-treatment. Moreover, the potential underlying mechanisms were uncovered, and we illustrated that sevoflurane promoted GSK-3ß activation in LPS-treated ALI mice lung tissues, and re-activation of GSK-3ß by the PI3K/Akt pathway inhibitor LY294002 suppressed LPS-induced pyroptotic cell death in vivo. Consistently, in the in vitro macrophages, our data hinted that LPS-induced pyroptotic cell death were also reversed by sevoflurane. Collectively, the above results suggest that sevoflurane re-activated GSK-3ß to suppress LPS-induced pyroptotic cell death, inflammation and ALI.


Assuntos
Lesão Pulmonar Aguda , Lipopolissacarídeos , Lesão Pulmonar Aguda/induzido quimicamente , Lesão Pulmonar Aguda/tratamento farmacológico , Lesão Pulmonar Aguda/metabolismo , Animais , Glicogênio Sintase Quinase 3 beta/metabolismo , Inflamassomos/metabolismo , Inflamação/tratamento farmacológico , Lipopolissacarídeos/farmacologia , Camundongos , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Inibidores de Fosfoinositídeo-3 Quinase , Fosforilação , Piroptose , Sevoflurano/uso terapêutico
11.
Biomed Res Int ; 2022: 9339824, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35615010

RESUMO

Postoperative cognitive dysfunction (POCD) in elderly patients undergoing general anesthesia is a major problem in the aging society. Sevoflurane is the most widely applied anesthetic in clinical practice. In this study, we investigated the effects of the GLP-1 analogue liraglutide on cognitive function in aged rats anesthetized by sevoflurane. Specifically, 48 Sprague-Dawley rats were divided into the control (C) group, the liraglutide (L) group, the sevoflurane (S) group, and the sevoflurane+liraglutide (SL) group, each group with 12 rats. In the S group and the SL group, the rats were injected subcutaneously with normal saline and liraglutide after inhalation of a mixture of 3% sevoflurane and pure oxygen. In the C group and the L group, normal saline and liraglutide were injected subcutaneously into the rats after inhalation of pure oxygen. Morris Water Maze Task was applied for the detection of spatial learning and memory in rats; HE and TUNEL for staining; and western blot for quantifying Bax, Bcl-2 expression, and examining caspase-3 activity in hippocampal tissues as well as for revealing the antiapoptotic mechanism. Besides, the accumulation of inflammatory factors NF-κB and IL-1ß in the hippocampal tissue was quantitatively studied to reveal the anti-inflammatory mechanism. The protective effect of liraglutide on sevoflurane toxicity was the first to be confirmed in this study. Additionally, this study elucidated the mechanism of the above effect. The results of this study might be helpful to find an effective medical solution for the treatment of POCD caused by sevoflurane anesthesia.


Assuntos
Anestésicos Inalatórios , Disfunção Cognitiva , Idoso , Anestésicos Inalatórios/farmacologia , Anestésicos Inalatórios/uso terapêutico , Animais , Disfunção Cognitiva/tratamento farmacológico , Disfunção Cognitiva/metabolismo , Hipocampo/metabolismo , Humanos , Liraglutida/farmacologia , Aprendizagem em Labirinto , Oxigênio/metabolismo , Ratos , Ratos Sprague-Dawley , Solução Salina/farmacologia , Sevoflurano/farmacologia , Sevoflurano/uso terapêutico
12.
Biochem Biophys Res Commun ; 614: 175-182, 2022 Jul 23.
Artigo em Inglês | MEDLINE | ID: mdl-35598428

RESUMO

Maternal exposure to anesthetic agents could impose significant neurocognitive risks on the developing brain of infants. Myelin produced by oligodendrocytes (OLs) is essential for the development of brain. However, the concrete effect of general anesthesia on the development and myelination of OLs is still elusive. In this study, we aim to investigate postnatal myelination and neural behavior after maternal exposure to sevoflurane. Pregnant C57BL/6 J mice (gestational day 15.5) were anesthetized with 2.5% sevoflurane (in 97.5% O2) for 6 h. Cognitive function and motor coordination of the offspring mice were evaluated with novel object recognition, Morris water maze and accelerating rotarod tests. Myelination and development of hippocampal OLs were analyzed with immunohistochemistry, qRT-PCR, western blotting and electron microscopy. The functionality of myelin was measured with electrophysiology. Our results showed that sevoflurane anesthesia during the gestational period induced cognitive and motor impairments in offspring mice, accompanied with damages of myelin structure and down regulations of myelin-associated genes and proteins (including MBP, Olig1, PDGFRα, Sox10, etc.). The development and maturation of OLs were suppressed, and the axonal conduction velocity was declined. These results demonstrated that maternal sevoflurane exposure could induce detrimental effects on cognitive and motor functions in offspring, which might be associated with disrupted myelination of OLs in the hippocampus.


Assuntos
Exposição Materna , Transtornos Motores , Animais , Cognição , Feminino , Hipocampo/metabolismo , Humanos , Exposição Materna/efeitos adversos , Camundongos , Camundongos Endogâmicos C57BL , Transtornos Motores/induzido quimicamente , Bainha de Mielina , Oligodendroglia/fisiologia , Gravidez , Sevoflurano/efeitos adversos
13.
Exp Cell Res ; 417(1): 113217, 2022 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-35598654

RESUMO

Whether and how sevoflurane preconditioning (SevoPre) exerts protection against acute myocardial ischemia/reperfusion (MI/R) injury remains elusive. We observed significant myocardial injury, as evidenced by infarct size, cardiomyocyte apoptosis, and circulating troponin-I, at 3 h of MI/R in both wildtype and adiponectin knockout mice. The injury was significantly ameliorated by SevoPre in wildtype mice, but not in adiponectin knockout mice. In wildtype mice, we found that MI/R could increase endoplasmic reticulum stress of cardiomyocytes, and impair association of adiponectin receptor 1 and ceveolin-3, both of which processes were largely restored by SevoPre. In summary, we demonstrated that significant injury had already took place at 3 h of MI/R, which could be ameliorated by SevoPre via promoting affinity of adiponectin receptor 1 and ceveolin-3, and then attenuating endoplasmic reticulum stress of cardiomyocytes.


Assuntos
Traumatismo por Reperfusão Miocárdica , Adiponectina/genética , Animais , Apoptose , Estresse do Retículo Endoplasmático , Camundongos , Camundongos Knockout , Traumatismo por Reperfusão Miocárdica/prevenção & controle , Miócitos Cardíacos , Receptores de Adiponectina/genética , Sevoflurano/farmacologia
14.
Oxid Med Cell Longev ; 2022: 9771743, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35528522

RESUMO

Cerebral ischemia reperfusion injury (IRI) induced by hemorrhagic shock and reperfusion (HSR) is the main cause of death following trauma. Previous studies indicated the neuroprotective effect of sevoflurane postconditioning (SP) in cerebral IRI. However, the mechanisms still remain elusive. Cerebral IRI models with SP were established by using HSR with C57BL/6 mice (male, 3-month-old) in vivo and by using oxygen glucose deprivation and reoxygenation (OGD/R) with HT22 cells in vitro. Postoperative cognition was evaluated by the Morris water maze, novel object recognition, and elevated plus maze tests. The role of SIRT1 was determined by using siRNA, a sensitive inhibitor (EX527), or an overexpression shRNA-GFP lentivirus. IRI caused significant disabilities of spatial learning and memory associated with enhanced cerebral infarct and neuronal apoptosis, which were effectively attenuated by SP. IRI also made a significant decrease of SIRT1 accompanied by oxidative stress, mitochondria dysfunction, and inactivated autophagy. SP or genetically overexpressing SIRT1 significantly suppressed defective autophagy, mitochondrial oxidative injury, and neuronal death caused by HSR or OGD/R. However, genetic suppression or pharmacological inhibition of SIRT1 significantly reversed the impact of SP treatment on mitochondrial DNA transcription ability and autophagy. Our results demonstrate that the loss of SIRT1 causes a sequential chain of mitochondrial dysfunction, defective autophagy, and neuronal apoptosis after IRI in the preclinical stroke models. Sevoflurane postconditioning treatment could effectively attenuate pathophysiological signatures induced by noxious stimuli, which maybe mediated by SIRT1.


Assuntos
Disfunção Cognitiva , Traumatismo por Reperfusão , Choque Hemorrágico , Animais , Apoptose , Autofagia , Disfunção Cognitiva/complicações , Disfunção Cognitiva/tratamento farmacológico , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Mitocôndrias , Traumatismo por Reperfusão/complicações , Traumatismo por Reperfusão/tratamento farmacológico , Sevoflurano/farmacologia , Choque Hemorrágico/complicações , Choque Hemorrágico/tratamento farmacológico , Sirtuína 1
15.
Hum Exp Toxicol ; 41: 9603271221102519, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35575159

RESUMO

Anesthesia may induce neuronal tau phosphorylation and neurotoxicity in the developing brain. Apolipoprotein E (ApoE) may play a protective role in neuronal activity and injury repair, whereas its 18-kDa fragments are reported to induce neurodegeneration and neuroinflammation in Alzheimer's disease patients. We aimed to test the hypothesis that differences in 18-kDa ApoE fragment levels, but not full-length ApoE, in primary neurons contribute to differences in tau phosphorylation and neuroinflammation with or without sevoflurane administration. Neurons extracted from wild-type (WT), ApoE knockout (ApoE-KO), and ApoE ε3-and ε2-targeted replacement (ApoE ε3, ApoE ε2) mice were divided into control and sevoflurane groups. Neurons in the sevoflurane group were treated with 21% O2, 5% CO2, and 4.1% sevoflurane, whereas those in the control group were treated with 21% O2 and 5% CO2 only on day 5 of neuronal culture. ApoE mRNA, full-length ApoE, 18-kDa ApoE fragments, Tau-PS202/PT205 (AT8), Tau-PSer396/404 (PHF1), tumor necrosis factor (TNF)-α, and interleukin (IL)-6 and IL-1ß levels were measured. The data showed that sevoflurane-induced AT8 and PHF1 increases, and TNF-α, IL-6, and IL-1ß increases in WT or ApoE ε3 neurons (both expressing full-length and 18-kDa fragmented ApoE) could be mitigated in ApoE ε2 (only expressing full-length ApoE), but not in ApoE-KO neurons, indicating that differences in 18-kDa ApoE fragments, but not full-length ApoE, in primary mouse neurons contributed to differences in tau phosphorylation and neuroinflammation with or without 4.1% sevoflurane administration.


Assuntos
Anestésicos , Síndromes Neurotóxicas , Animais , Apolipoproteína E2 , Apolipoproteína E3/genética , Apolipoproteínas E/genética , Apolipoproteínas E/metabolismo , Dióxido de Carbono , Humanos , Interleucina-6 , Camundongos , Fosforilação , Sevoflurano , Fator de Necrose Tumoral alfa
16.
PLoS One ; 17(5): e0268473, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35559987

RESUMO

BACKGROUND: Previous studies have shown that the anesthetic technique may influence long-term outcomes after cancer surgery. However, the association between the anesthetic technique and long-term oncological outcomes after oral cancer surgery remains unclear. Therefore, we conducted this study to address this gap. METHODS: We reviewed the electronic medical records of patients who underwent elective oral cancer surgery between January 2014 and December 2015. The patients were grouped based on the anesthesia maintenance: either propofol or sevoflurane. Propensity score matching in a 1:1 ratio was performed to deal with the potential confounding effects of baseline characteristics. Univariate and multivariate Cox regression analyses were performed to compare hazard ratios (HRs) and identify the risk factors for death and recurrence. Survival analysis was performed using the Kaplan-Meier method, and survival curves were constructed from the date of surgery to death. RESULTS: In total, 1347 patients were eligible for analysis, with 343 and 1004 patients in the propofol and sevoflurane groups, respectively. After propensity score matching, 302 patients remained in each group. Kaplan-Meier survival curves demonstrated the 5-year overall and recurrence-free survival rates of 59.3% and 56.0% and 62.7% and 56.5% in the propofol and sevoflurane groups, respectively. There was no significant difference in overall survival or recurrence-free survival between the groups. The multivariate Cox analysis verified this conclusion with HRs of 1.10 and 1.11 for overall survival and recurrence-free survival, respectively, in the sevoflurane group. Older age, advanced tumor-node-metastasis (TNM) stage, and American Society of Anesthesiologists class III were associated with poor overall survival. Patients with advanced TNM stage and poorly differentiated squamous cell carcinoma had a higher recurrence risk than their counterparts. CONCLUSION: The overall and recurrence-free survival rates were similar between propofol-based intravenous anesthesia and sevoflurane volatile anesthesia in patients who underwent oral cancer surgery.


Assuntos
Anestésicos Inalatórios , Neoplasias Bucais , Propofol , Anestesia por Inalação , Anestesia Intravenosa , Anestésicos Intravenosos , Desflurano , Humanos , Neoplasias Bucais/cirurgia , Estudos Retrospectivos , Sevoflurano
17.
BMC Anesthesiol ; 22(1): 148, 2022 May 16.
Artigo em Inglês | MEDLINE | ID: mdl-35578184

RESUMO

OBJECTIVE: The goal of this study was to compare the end-tidal sevoflurane concentration and time for intravenous cannulation at induction of anesthesia using sevoflurane with or without nitrous oxide in healthy children and in those with developmental disabilities. METHODS: Normal and developmentally disabled children were anesthetized by inhalation of sevoflurane with nitrous oxide or with nitrous oxide-free oxygen, and intravenous cannulae were introduced. Nitrous oxide was stopped after loss of consciousness. The following parameters were recorded for each patient: age, gender, height, weight, BMI, duration of intravenous cannulation, end-tidal concentration of sevoflurane at the completion of intravenous cannulation, and use of nitrous oxide. For each parameter except gender, p-value were calculated by one-way analysis of variance (ANOVA). For gender, p-value were calculated using the Fisher method. Two-way ANOVA was performed to evaluate the effect of patient health status and nitrous oxide use on the end-tidal concentrations of sevoflurane and the time required for intravenous cannulation. RESULTS: The end-tidal sevoflurane concentrations at the completion of the intravenous cannulation had received a significant main effect of the factor "the use of nitrous oxide" (F(1,166) = 25.8, p < 0.001, η2 = 0.13) and a small effect of the factor "the patient health status" (F(1,166) = 0.259, p = 0.611, η2 = 0.001). However, the time required for intravenous cannulation was not significantly affected by either of the two factors, "the use of nitrous oxide" (F(1,166) = 0.454, p = 0.501, η2 = 0.003) and "the patient health status" (F(1,166) = 0.308, p = 0.579, η2 = 0.002). CONCLUSIONS: Between the healthy children and the children with developmental disabilities, no significant differences in the time required for the intravenous cannulation from the beginning of anesthetic induction. However, the end-tidal sevoflurane concentrations at the completion of the intravenous cannulation was significantly different. Sevoflurane in alveoli might be diluted by nitrous oxide.


Assuntos
Anestésicos Inalatórios , Éteres Metílicos , Anestesia por Inalação , Anestésicos Inalatórios/farmacologia , Cateterismo , Criança , Deficiências do Desenvolvimento , Humanos , Óxido Nitroso , Sevoflurano
18.
Khirurgiia (Mosk) ; (5): 52-58, 2022.
Artigo em Russo | MEDLINE | ID: mdl-35593628

RESUMO

OBJECTIVE: To study the dynamics of markers of brain damage, determine their role in postoperative cognitive dysfunction (POCD) and evaluate the effectiveness of therapeutic correction of POCD in patients undergoing laparoscopic cholecystectomy under inhalation anesthesia with sevoflurane. MATERIAL AND METHODS: We analyzed data of two representative groups of patients (aged 55 years and older) who underwent laparoscopic cholecystectomy under inhalation anesthesia with sevoflurane. Perioperative neuropsychological testing was performed for monitoring of higher mental functions (MoCA and FAB). In the 1st group (n=30), POCD was not corrected. In the 2nd group (n=30), Cellex 0.1 mg was subcutaneously injected once before surgery and then throughout 5 postoperative days to correct cognitive disorders. RESULTS: Neuropsychological testing revealed moderate POCD in the 1st group. In the 2nd group, Cellex provided a significantly lower level of brain-specific proteins compared to the 1st group. This limited brain damage and ensured no severe cognitive deficit in early postoperative period. CONCLUSION: Laparoscopic cholecystectomy under inhalation anesthesia with sevoflurane in patients aged 55 years and older is accompanied by moderate POCD in early postoperative period. Injections of Cellex 0.1 mg before surgery and then for 5 postoperative days prevent POCD and improve quality of life.


Assuntos
Anestésicos Inalatórios , Colecistectomia Laparoscópica , Disfunção Cognitiva , Anestesia por Inalação/efeitos adversos , Anestésicos Inalatórios/efeitos adversos , Colecistectomia Laparoscópica/efeitos adversos , Disfunção Cognitiva/diagnóstico , Disfunção Cognitiva/etiologia , Humanos , Complicações Pós-Operatórias/diagnóstico , Complicações Pós-Operatórias/etiologia , Complicações Pós-Operatórias/prevenção & controle , Qualidade de Vida , Sevoflurano/efeitos adversos
19.
Neurotoxicology ; 90: 256-264, 2022 May.
Artigo em Inglês | MEDLINE | ID: mdl-35472370

RESUMO

Prolonged sevoflurane exposure leads to neurotoxicity. Autophagy plays an important role in promoting cell survival in different conditions. However, the role and mechanism of autophagy in sevoflurane-induced neurotoxicity were not fully elucidated. We attempted to indicate whether sevoflurane could activate the AMP-activated protein kinase (AMPK)/mechanistic target of rapamycin (mTOR)-mediated autophagy to attenuate anesthetics-induced neuronal injury in this study. Sevoflurane treatment significantly decreased the cell viability and induced apoptosis of SH-SY5Y cells. The expression level of Bcl-2 decreased, while that of Bax remarkably increased. Meanwhile, autophagy was activated by sevoflurane exposure as evidenced by increased expression levels of autophagy-related proteins (LC3-II and Atg5), decreased expression level of autophagic substrate P62, and increased autophagosomes and autolysosomes. Further autophagosomes and fewer autolysosomes were observed in the presence of Bafilomycin A1, an autolysosomes degradation inhibitor, suggesting that sevoflurane induced autophagic flux rather than inhibiting degradation of autophagy. Activation of autophagy by rapamycin partly reversed the sevoflurane-decreased cell viability. In contrast, inhibition of autophagy by 3-Methyladenine (3-MA) or Atg5-targeted small interfering RNA (siRNA) aggravated the sevoflurane-induced neurotoxicity. Further examination revealed that sevoflurane-induced autophagy was mediated by the AMPK/mTOR signaling pathway, with increased p-AMPK expression and decreased p-mTOR expression. Collectively, these results indicated that sevoflurane activates autophagy by regulating the AMPK/mTOR signaling pathway, which is protective against sevoflurane-induced damage in SH-SY5Y cells. Our results may assist clinicians to develop further promising therapeutic strategies for the neurotoxicity induced by inhaled anesthetics.


Assuntos
Proteínas Quinases Ativadas por AMP , Neuroblastoma , Proteínas Quinases Ativadas por AMP/genética , Proteínas Quinases Ativadas por AMP/metabolismo , Apoptose , Autofagia , Linhagem Celular Tumoral , Humanos , Neuroblastoma/metabolismo , Sevoflurano/farmacologia , Transdução de Sinais , Sirolimo/farmacologia , Serina-Treonina Quinases TOR
20.
Int J Dev Neurosci ; 82(4): 339-348, 2022 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-35362638

RESUMO

The current study aimed to examine the effects of echinacoside on cognitive impairment in mice after exposure to sevoflurane. To examine the role of FOXO1, si-FOXO1 and si-con were injected into the hippocampus through the left lateral cerebral ventricles. Sevoflurane-induced mice had serious cognitive dysfunction. However, pretreatment with echinacoside alleviated the cognitive dysfunction, as measured by a shortened escape latency time, and increased platform crossing times, the percentage of distance in the target quadrant and Y-maze spontaneous alternations. In addition, we found that echinacoside elevated FOXO1 expression in the hippocampus; increased the expression of autophagy-related proteins including Beclin 1, ATG5, ATG7, and LC3; and reduced P62 expression. Silencing of FOXO1 aggravated the cognitive deficits and reduced expression of the autophagy-related markers, whereas the effects of si-FOXO1 on memory were abrogated by echinacoside. Echinacoside attenuated the cognitive impairment in sevoflurane-induced mice through FOXO1-mediated autophagy.


Assuntos
Disfunção Cognitiva , Proteína Forkhead Box O1 , Animais , Autofagia , Disfunção Cognitiva/tratamento farmacológico , Disfunção Cognitiva/metabolismo , Disfunção Cognitiva/patologia , Proteína Forkhead Box O1/metabolismo , Hipocampo/metabolismo , Hipocampo/patologia , Camundongos , Sevoflurano/efeitos adversos
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