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Objective:To evaluate the effect of dexamethasone combined with aminophylline on perioperative airway responses in COVID-19 convalescent patients undergoing gynecological laparoscopic surgery.Methods:Sixty-eight COVID-19 convalescent patients, aged 25-57 yr, of American Society of Anesthesiologists Physical Status classification Ⅰ or Ⅱ, undergoing gynecological laparoscopic surgery, were divided into experimental group ( n=34) and control group ( n=34). In experimental group, dexamethasone 10 mg was intravenously injected at the beginning of anesthesia induction, and aminophylline 0.25 g (in 100 ml of normal saline) was intravenously infused for 10 min starting from 15 min before the end of surgery. In control group, the equal volume of normal saline was administrated instead at the same time point. Airway secretions, laryngospasm and bronchospasm were recorded from the time point before operation to 24 h after operation, and coughing was also recorded from emergence to 3 min after extubation. The blood eosinophils (EOS) count, percentage of EOS (EOS%), and neutrophil to lymphocyte ratio were determined, and plasma C reactive protein level was measured by enzyme-linked immunosorbent assay before operation and at 24 h after operation. The serum levels of interleukin-6, tumor necrosis factor-α and interferon-γ were measured before operation, at 5 and 10 min after extubation and at 24 h after operation. Results:Compared with control group, the incidence of coughing, severity of coughing, incidence of increased airway secretion, and grade of airway secretion were significantly decreased, the levels of EOS, EOS%, neutrophil to lymphocyte ratio and plasma C reactive protein in peripheral blood and serum levels of interferon-γ, interleukin-6 and tumor necrosis factor-α were significantly decreased after operation ( P<0.05), and no significant change was found in the incidence of bronchial spasm in experimental group ( P>0.05). No laryngeal spasm occurred in both groups. Conclusions:Dexamethasone combined with aminophylline can relieve the perioperative airway responses by inhibition of inflammatory responses in COVID-19 convalescent patients undergoing gynecological laparoscopic surgery.
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Objective:To explore the improvement and its mechanism of minocycline on sevoflurane anesthesia induced cognitive dysfunction in aged mice.Methods:Totally 75 aged clean-grade C57BL/6 mice were randomly divided into control (Con) group( n=25), sevoflurane (Sev) group( n=25) and sevoflurane + minocycline (Sev+ Min) group( n=25). Anesthetic injury was induced by 3% sevoflurane (2 h/d for 3 days) in Sev group. Minocycline (50 mg/kg) was injected intraperitoneally first, and then 3% sevoflurane (2 h/d for 3 days) anesthesia was performed in Sev+ Min group. Saline alone was injected intraperitoneally (once a day for 3 days) in Con group.The spatial memory function was detected by Morris water maze experiments. BrdU was used to label new neuron and the proliferation was observed by immunohistochemistry. The field excitatory postsynaptic potential (fEPSP) slope was measured in hippocampal dentate gyrus (DG) region of isolated brain slices by electricphysiological technique.The data were analyzed by repeated measures analysis of variance and SNK-q test using SPSS 21.0 software. Results:Results from positioning navigation experiment showed that the group×time interaction effect of mice was significant( F=15.65, P<0.01). On the 6th day after anesthesia, compared with Con group, the escape latency of the original platform in Sev group was significantly increased ( q=4.35, P<0.05) in space exploration experiment, while the target quadrant time ratio ( q=6.15, P<0.05))and the mean annulus crossings ( q=6.45, P<0.05) were significantly decreased. Compared with Sev group, the escape latency in Sev+ Min group was significantly decreased ( q=3.01, P<0.05), while the target quadrant time ratio ( q=3.21, P<0.05) and the mean annulus crossings ( q=3.48, P<0.05) were significantly increased. In immunohistochemistry experiment, the number of BrdU positive cells in Sev group was significantly reduced ((227.45±43.25), q=8.67, P<0.01) compared with Con group (355.87±62.58). Compared with Sev group, the number of BrdU positive cells in Sev+ Min group was significantly increased ((338.73±47.27), q=8.68, P<0.01). In electricphysiological test, the fEPSP slope after high frequency stimulation in Sev group ((126.83±25.67)%, q=6.18, P<0.01)) was significantly lower than that in Con group((214.38±43.42)%). In Sev+ Min group, the fEPSP slope was significantly higher ((178.49±32.67)%, q=3.64, P<0.05) than that in Sev group. Conclusion:Sevoflurane anesthesia can induce the short-term cognitive dysfunction in aged mice, and its mechanism is related to inhibiting neuron proliferation and synaptic plasticity. Minocycline can alleviate the damage caused by sevoflurane.
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Objective To investigate the effect of sevoflurane anesthesia on learning and memory in mice and the relationship with histone acetylation. Methods Thirty-six adult male C57BL/6 mice were ran-domly divided into control group(mice inhaled 95％ O2 for 6 h), sevoflurane (Sevo) group (1. 5％ Sevo group, 2％ Sevo group, 3％ Sevo group:mice inhaled 1. 5％, 2％ and 3％ sevoflurane for 6 h respectively) , sevoflurane + SAHA (Sevo + SAHA) group (mice were intraperitoneally injected with histone deacetylase inhibitor SAHA ( 25 mg/kg) . And 1 h later, 3％ Sevo was inhaled continuously for 6 hours. ) and SAHA group(mice were intraperitoneally injected with histone deacetylase inhibitor SAHA (25 mg/kg)). The abil-ity of learning and memory in mice was estimated by Morris water maze. The expression levels of Ac-H3, BDNF and Syt-I protein in the hippocampus were detected by Western blot. Results In Morris water maze, 3％ sevoflurane anesthesia significantly prolonged the escape latency((46. 91±1. 84)s),and significantly decreased the ratio of target time((35. 84±5. 40)％) compared with that of control group((23. 46±2. 67)s, (49. 74±4. 91)％,P<0. 05). Compared with 3％ Sevo group,the ratio of target time in Sevot+SAHA group ((46. 86±4. 37)％) was increased(P<0. 05). Moreover,3％ sevoflurane anesthesia significantly decreased the expression levels of Ac-H3 (10. 23±2. 45),BDNF (6. 72±1. 21) and Syt-I (8. 25±2. 11) in the hippo-campus compared with that of control group((15. 45±2. 58),(10. 17±1. 45) and (15. 02±3. 38),P<0. 05) . However,pre-administration of the histone deacetylase inhibitor SAHA significantly increased the ra-tio of target time in Morris water maze,and improved the expression levels of Ac-H3 (14. 06±2. 79),BDNF (10. 13±1. 06) and Syt-I (14. 16±3. 66) in Sevo+SAHA group compared with that of Sevo group (P<0. 05) . Conclusion The high dose of sevoflurane anesthesia can induce learning and memory impairment through the inhibitation of histone acetylation in the hippocampus.
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ObjectiveTo investigate the effects of sevoflurane on short-term memory impairment and the relative synaptic mechanism.MethodsAt 12 h,24 h and 72 h after the mice were exposed to 1.5％ sevoflurane for 1h,the spontaneous alternation and locomotor activity was assessed by Y maze,the short term potentiation (STP) were measured with extracellular recording technique in hippocampal slices.ResultsAt 12h after administration with sevoflurane in vivo,the spontaneous alternation ( (54.7 ± 1.7) ％,P＜0.01 ) and locomotor activity (16.4 ± 1.3,P ＜ 0.01 ) decreased significantly compared with that of control group,and the population spike amplitude after induction of STP ( ( 122.3 ± 13.9) ％,P ＜ 0.05 ) decreased significantly in hippocampal slices,but there was no different at 24h and 72h.After administration with sevoflurane in vitro,the basic ( ( 83.5 ± 8.9) ％,P ＜ 0.01 ) or titanic ( ( 116.5 ± 14.9) ％,P ＜ 0.01 ) population spike amplitude decreased significantly in hippocampal slices,but the amplitude could recovery after wash-out.ConclusionSevoflurane can impair the shortterm memory by suppressing synaptic transmission in the near future but not the long future.
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BACKGROUND: Lidocaine is deemed to can attenuate the inflammatory response, but the mechanisms are poorly understood. Nuclear factor-κB (NF-κB) is a key process of imflammatory response. OBJECTIVE: To determine the effect of lidocaine on activation and apoptosis of NF-κB in human neutrophiis in vitro. DESIGN, TIME AND SETTING: The controlled experiment was conducted at the Jiangsu Provincial Key Laboratory of Anesthesiology from October 2006 to February 2007. MATERIALS: Tumor necrosis factor (TNF)-α (0127:B8) was purchased from Sigma, USA. Peripheral blood samples were obtained from healthy donors after their informed consent. METHODS: Human neutrephilic granulocytes were assigned into five groups: ① saline control, ② TNF-α, ③ TNF-α+ lidocaine 1.0 mmol/L, ④ TNF-α+ lidocaine 2.0 mmol/L, and ⑤ TNF-α+ lidocaine 4.0 mmol/L groups. Incubation wasperformed for 3 hours.MAIN OUTCOME MEASURES: The effects of lidocaine on expression of NF- κB mRNA and I- κB mRNA in the cytosol extracts were analyzed by reverse transcription-polymerase chain reaction (RT-PCR), and content of p65 protein were analyzed by Western blot. Neutrophilic granulocyte apoptosis was detected on flow cytomatry after incubation 12 hours and 24 hours.RESULTS: The expression of NF- κB mRNA in the nuclear extracts was significantly decreased and I- κB mRNA in the cytosoI extracts was markedly increased in the lidocaine group. The expression of NF- κB was significantly better in the 2.0 mmol/L and 4.0 mmol/L lidocaine groups than in the 1.0 mmol/L lidocaine group (P< 0.05). No significant difference was detected between the 2.0 mmol/L lidocaine group and the 4.0 mmol/L lidocaine group (P0.05). Lidocaine could significantly inhibit peripheral blood neutrophilic granulocyte apoptosis induced by TNF-α (p < 0.05). The inhibitory effect was significantly better in the 4.0 mmol/L lidocaine group than in the 1.0 mmol/L lidocaine group (P < 0.05). CONCLUSION: Lidocaine (1.0, 2.0 and 4.0 mmol/L) can down-regulate the expressions of NF- κB subunit p65 mRNA and the content of p65 protein in human polymorphoneclear neutrophils, and can significant reverse the reduction of apoptosis induced by TNF-α.