PDF(Pubmed)
Abstract：
UNASSIGNED: Etomidate can induce myoclonus with an incidence of 50 ~ 85% during anesthesia induction. Dexamethasone, as a long-acting synthetic glucocorticoid, has neuroprotective effects. However, the effects of dexamethasone on the etomidate-induced myoclonus remain uncertain.
UNASSIGNED: Adult male Sprague-Dawley rats were randomly assigned to receive etomidate (1.5 mg/kg) plus dexamethasone (4 mg/kg) (etomidate plus dexamethasone group) or etomidate (1.5 mg/kg) plus the same volume of normal saline (NS) (etomidate plus NS group). The mean behavioral scores, local field potentials and muscular tension were recorded to explore the effects of dexamethasone on etomidate-induced myoclonus. Liquid chromatography coupled with tandem mass spectrometric system (LC-MS/MS), quantitative real-time polymerase chain reaction (qRT-PCR), and western blotting were applied to analyze the levels of glutamate and γ-aminobutyric acid (GABA), the mRNA and protein expression of excitatory amino acid transporters (EAATs), and plasma corticosterone levels at different time points after anesthesia.
UNASSIGNED: Compared with the etomidate plus NS treatment, the etomidate plus dexamethasone treatment significantly decreased the mean behavioral score at 1, 3, 4, and 5 min after administration; the peak power spectral density (PSD) (p = 0.0197) in the analysis of ripple waves; and the glutamate level (p = 0.0139) in the neocortex. However, compared with etomidate plus NS, etomidate plus dexamethasone increased the expression of the neocortical proteins of EAAT1 (p = 0.0207) and EAAT2 (p = 0.0022) and aggravated the inhibition of corticosterone at 4 h (p = 0.0019), 5 h (p = 0.0041), and 6 h (p = 0.0009) after administration.
UNASSIGNED: Dexamethasone can attenuate the myoclonus, inhibit the glutamate accumulation, and reverse the suppression of EAATs in the neocortex induced by etomidate following myoclonus, while conversely aggravating etomidate-induced adrenal suppression.
UNASSIGNED: Adult male Sprague-Dawley rats were randomly assigned to receive etomidate (1.5 mg/kg) plus dexamethasone (4 mg/kg) (etomidate plus dexamethasone group) or etomidate (1.5 mg/kg) plus the same volume of normal saline (NS) (etomidate plus NS group). The mean behavioral scores, local field potentials and muscular tension were recorded to explore the effects of dexamethasone on etomidate-induced myoclonus. Liquid chromatography coupled with tandem mass spectrometric system (LC-MS/MS), quantitative real-time polymerase chain reaction (qRT-PCR), and western blotting were applied to analyze the levels of glutamate and γ-aminobutyric acid (GABA), the mRNA and protein expression of excitatory amino acid transporters (EAATs), and plasma corticosterone levels at different time points after anesthesia.
UNASSIGNED: Compared with the etomidate plus NS treatment, the etomidate plus dexamethasone treatment significantly decreased the mean behavioral score at 1, 3, 4, and 5 min after administration; the peak power spectral density (PSD) (p = 0.0197) in the analysis of ripple waves; and the glutamate level (p = 0.0139) in the neocortex. However, compared with etomidate plus NS, etomidate plus dexamethasone increased the expression of the neocortical proteins of EAAT1 (p = 0.0207) and EAAT2 (p = 0.0022) and aggravated the inhibition of corticosterone at 4 h (p = 0.0019), 5 h (p = 0.0041), and 6 h (p = 0.0009) after administration.
UNASSIGNED: Dexamethasone can attenuate the myoclonus, inhibit the glutamate accumulation, and reverse the suppression of EAATs in the neocortex induced by etomidate following myoclonus, while conversely aggravating etomidate-induced adrenal suppression.
摘要：
■依托咪酯可在麻醉诱导过程中诱发肌阵颤，发生率为50〜85％。地塞米松,作为一种长效合成糖皮质激素，具有神经保护作用。然而,地塞米松对依托咪酯诱导的肌阵颤的影响尚不确定.
■成年雄性Sprague-Dawley大鼠随机分配接受依托咪酯（1.5mg/kg）加地塞米松（4mg/kg）（依托咪酯加地塞米松组）或依托咪酯（1.5mg/kg）加相同体积的生理盐水（NS）（依托咪酯加NS组）。平均行为得分，记录局部场电位和肌张力,以探讨地塞米松对依托咪酯诱导的肌阵挛症的影响.液相色谱-串联质谱系统(LC-MS/MS)定量实时聚合酶链反应（qRT-PCR），应用蛋白质印迹法分析谷氨酸和γ-氨基丁酸（GABA）的水平，兴奋性氨基酸转运蛋白（EAATs）的mRNA和蛋白表达，麻醉后不同时间点血浆皮质酮水平。
■与依托咪酯加NS治疗相比，依托咪酯+地塞米松治疗显著降低了给药后1,3,4和5分钟的平均行为评分;波纹波分析中的峰值功率谱密度(PSD)(p=0.0197);新皮质中的谷氨酸水平(p=0.0139).然而,与依托咪酯加NS相比，依托咪酯加地塞米松增加了EAAT1（p=0.0207）和EAAT2（p=0.0022）的新皮质蛋白的表达，并在4h时加重了皮质酮的抑制（p=0.0019），5小时（p=0.0041），和给药后6小时（p=0.0009）。
■地塞米松可以减轻肌阵挛症，抑制谷氨酸的积累，并逆转由依托咪酯诱导的新皮质中EAAT的抑制，而反过来加重依托咪酯诱导的肾上腺抑制。
■成年雄性Sprague-Dawley大鼠随机分配接受依托咪酯（1.5mg/kg）加地塞米松（4mg/kg）（依托咪酯加地塞米松组）或依托咪酯（1.5mg/kg）加相同体积的生理盐水（NS）（依托咪酯加NS组）。平均行为得分，记录局部场电位和肌张力,以探讨地塞米松对依托咪酯诱导的肌阵挛症的影响.液相色谱-串联质谱系统(LC-MS/MS)定量实时聚合酶链反应（qRT-PCR），应用蛋白质印迹法分析谷氨酸和γ-氨基丁酸（GABA）的水平，兴奋性氨基酸转运蛋白（EAATs）的mRNA和蛋白表达，麻醉后不同时间点血浆皮质酮水平。
■与依托咪酯加NS治疗相比，依托咪酯+地塞米松治疗显著降低了给药后1,3,4和5分钟的平均行为评分;波纹波分析中的峰值功率谱密度(PSD)(p=0.0197);新皮质中的谷氨酸水平(p=0.0139).然而,与依托咪酯加NS相比，依托咪酯加地塞米松增加了EAAT1（p=0.0207）和EAAT2（p=0.0022）的新皮质蛋白的表达，并在4h时加重了皮质酮的抑制（p=0.0019），5小时（p=0.0041），和给药后6小时（p=0.0009）。
■地塞米松可以减轻肌阵挛症，抑制谷氨酸的积累，并逆转由依托咪酯诱导的新皮质中EAAT的抑制，而反过来加重依托咪酯诱导的肾上腺抑制。
