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Objective:To investigate the effects of dyclonine hydrochloride mucilage administered for oropharyngeal anesthesia on gag reflex in patients with chronic pharyngitis during gastroscopy.Methods:A total of 100 patients with chronic pharyngitis who met American Society of Anesthesiologists Classification I-II and received treatment in The First Affiliated Hospital of Ximen University from January to December 2020 were included in this study. Using the principle of voluntariness, these patients were divided into dyclonine hydrochloride mucilage (D) and control (C) groups, with 50 patients in each group. Ten minutes before anesthesia induction, patients in Group D took 10 mL of dyclonine hydrochloride mucilage in the mouth, but did not swallow it, and those in Group C were identically given equal volume of placebo. Ten minutes later, dyclonine hydrochloride mucilage or placebo was swallowed. For anesthesia induction, 20 μg Fentanyl and 2-4 mg/kg Propofol were intravenously administered. A gastroscopy examination was performed after the patient's consciousness disappeared. The patient's cough and body movement response scores during gastroscopy were recorded. Before anesthesia induction (T0), before endoscope insertion (T1), after endoscope insertion (T2), and after endoscope withdrawal (T3), mean arterial pressure and heart rate were recorded.Results:The incidence rate of cough and body movement in Group D were 20% (10/50) and 24% (12/50), which were significantly lower than 72% (36/50) and 68% (34/50) in Group C ( χ2 = 27.21, 19.49, both P < 0.001). At T1, mean arterial pressure in Group D and Group C was (62.21 ± 10.32) mmHg and (63.82 ± 10.51) mmHg(1 mmHg=0.133 kPa), respectively, which were significantly lower than (70.21 ± 13.13) mmHg and (70.91 ± 14.02) mmHg at T0 ( t = 3.15, 5.82, both P < 0.05). At T2, mean arterial pressure and heart rate in Group C were (80.13 ± 11.92) mmHg and (90.02 ± 15.63) beats/minute, respectively, which were significantly higher than (70.91 ± 14.02) mmHg and (78.75 ± 14.93) beats/minute at T0 in the same group ( t = 5.99, 4.03, both P < 0.05) and were also significantly higher than (66.21 ± 12.33) mmHg and (76.53 ± 10.31) beats/minute] at T2 in Group D ( t = 2.07, 2.67, both P < 0.05). Conclusion:Dyclonine hydrochloride mucilage administered for oropharyngeal anesthesia can effectively suppress gag reflex in patients with chronic pharyngitis and increase hemodynamic stability during gastroscopy.
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Objective:To investigate the effect of two different withdrawal sequences on the quality of recovery in patients undergoing nasal endoscopic surgery under combined intravenous and inhalation anesthesia.Methods:Seventy patients scheduled for endoscopic sinus surgery in The First Affiliated Hospital of Xiamen University, China from January to June 2019 were included in this study and randomly assigned to undergo intravenous anesthesia alone (Group A, n = 35) or combined intravenous and inhalation anesthesia (Group B, n = 35). Propofol 2-4 mg/kg, fentanyl 3-4 μg/kg, cisatracurium besylate 0.2 mg/kg were used to induce anesthesia. Propofol 4-6 mg/kg/h, remifentanil 6.5-13.0 mg/kg/h, sevoflurane ≥ 0.30 minimum alveolar concentration were used to maintain anesthesia. At 30 minutes before the end of surgery, inhalational sevoflurane administration and pump propofol administration were stopped in the groups A and B respectively. At 10 minutes before the end of surgery, pump propofol administration and inhalational sevoflurane administration were stopped in the groups A and B respectively. At the end of surgery, pump remifentanil administration was stopped in both groups A and B. The time to spontaneous breathing recovery, the time to consciousness recovery, and the time to tracheal extubation were recorded. Mean arterial pressure and heart rate were recorded at the time of entering the operation room (T0), at the end of anesthesia (T1), at the time of spontaneous breathing recovery (T2), consciousness recovery (T3) and tracheal extubation (T4), 5 minutes (T5) and 10 minutes after tracheal extubation (T6). Agitation score was recorded at T2-T6 and at 20 minutes after tracheal extubation (T7). Cough score was recorded at T4. Results:The time to spontaneous breathing recovery, the time to consciousness recovery, and the time to tracheal extubation in group A were (16.0 ± 4.6) minutes, (18.0 ± 5.3) minutes, (19.0 ± 5.5) minutes, respectively, which were significantly longer than (8.8 ± 3.5) minutes, (9.5 ± 4.1) minutes, (10.7 ± 4.5) minutes, respectively in the group B ( t = 9.554, 8.881, 9.011, all P < 0.05). There were no significant differences in mean arterial pressure and heart rate recorded at T0-T6 between groups A and B (all P > 0.05). There was no significant difference in agitation score measured at T3-T6 between groups A and B (all P > 0.05). There was no significant difference in cough score recorded at T4 between groups A and B ( P > 0.05). Conclusion:Two different withdrawal sequences can maintain stable hemodynamics and reduce agitation during recovery period and cough during extubation. The recovery time of remifentanil combined with propofol is longer than that of remifentanil combined with sevoflurane.
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BACKGROUND: Extracellular signal-regulated kinase 1/2 (ERK1/2) has been implicated in learning and memory; however, whether intravenous anesthetics modulate ERK1/2 remains unknown. The aim of this study was to examine the effect of several intravenous anesthetics on the phosphorylation of ERK1/2 in the hippocampus of adult mice. METHODS: Western blotting was used to examine cellular levels of phosphorylated and unphosphorylated ERK1/2 in mouse hippocampus slices, which were incubated with or without anesthetics including propofol, etomidate, ketamine and midazolam, a protein kinase C (PKC) activator or inhibitor, or phospholipase C (PLC) activator or inhibitor. RESULTS: Propofol, etomidate, ketamine and midazolam reduced phosphorylation of ERK1/2 in a time-dependent manner. Washing out propofol after 5 min increased ERK1/2 phosphorylation. The anesthetic-induced depression of ERK1/2 phosphorylation was blocked by 0.1 µM phorbol-12-myristate 13-acetate (an activator of PKC), 50 µM U73122 (an inhibitor of PLC). The anesthetic-induced depression of ERK1 phosphorylation was blocked by 1 mMN-methyl-d-aspartate (NMDA). Whereas 100 µM chelerythrine (an inhibitor of PKC) and 100 µM carbachol (an activator of PLC) and 20 µM PD-98059 (an inhibitor of MEK) had additive effects on propofol-induced inhibition of ERK1/2 phosphorylation. In contrast, 10 µM MK801 (a NMDA receptor antagonist) did not block anesthetic-induced inhibition of ERK1/2 phosphorylation. CONCLUSION: Intravenous anesthetics markedly decreased phosphorylation of ERK1/2 in mouse hippocampal slices, most likely via the NMDA receptor, and PLC- and PKC-dependent pathways. Thus, ERK1/2 represents a target for anesthetics in the brain.
