本文選題：麻醉 + 右美托咪定　； 參考：《山東醫(yī)藥》2017年28期

【摘要】：目的探討右美托咪定輔助氯胺酮麻醉對(duì)大鼠海馬區(qū)神經(jīng)細(xì)胞的保護(hù)作用。方法將32只SD大鼠按照隨機(jī)數(shù)字表法分為空白對(duì)照組、氯胺酮組、右美托咪定組和聯(lián)合用藥組,每組8只�？瞻讓�(duì)照組腹腔注射生理鹽水50 m L/kg,間隔5 min皮下注射生理鹽水50 m L/kg;氯胺酮組腹腔注射氯胺酮70 mg/kg,間隔5 min皮下注射生理鹽水50 m L/kg;右美托咪定組腹腔注射右美托咪定25μg/kg,間隔5 min皮下注射生理鹽水50 m L/kg;聯(lián)合用藥組腹腔注射氯胺酮70 mg/kg,間隔5 min皮下注射右美托咪定25μg/kg;各組均每天注射1次,連續(xù)注射3天。各組隨機(jī)取4只,檢測(cè)首次注射即刻(t0)及末次注射15、30、45、60、75、90 min(t1~t6)呼吸頻率、翻正反射消失時(shí)間、翻正反射消失持續(xù)時(shí)間以及夾尾反射完全消失時(shí)間,Morris水迷宮實(shí)驗(yàn)檢測(cè)各組訓(xùn)練1~5天的逃避潛伏期。各組剩余大鼠末次注射結(jié)束,斷頭處死,TUNEL法檢測(cè)海馬區(qū)神經(jīng)細(xì)胞凋亡率,Western blotting法檢測(cè)PKC、ERK1/2、Bcl-2蛋白表達(dá)。結(jié)果與聯(lián)合用藥組比較,氯胺酮組翻正反射消失時(shí)間明顯延長(zhǎng),鎮(zhèn)靜維持時(shí)間、翻正反射消失持續(xù)時(shí)間明顯縮短,兩組比較P均0.05。t1、t2、t3時(shí),氯胺酮組呼吸頻率均顯著高于空白對(duì)照組、右美托咪定組和聯(lián)合用藥組同時(shí)間(P均0.05)。空白對(duì)照組、右美托咪定組、聯(lián)合用藥組各時(shí)間逃避潛伏期比較P均0.05;訓(xùn)練第4、5天,氯胺酮組逃避潛伏期較空白對(duì)照組、右美托咪定組和聯(lián)合用藥組明顯延長(zhǎng)(P均0.05)。氯胺酮組神經(jīng)細(xì)胞凋亡率明顯高于空白對(duì)照組、右美托咪定組和聯(lián)合用藥組(P均0.05),而空白對(duì)照組、右美托咪定組和聯(lián)合用藥組神經(jīng)細(xì)胞凋亡率比較P均0.05。氯胺酮組海馬區(qū)PKC、ERK1/2、Bcl-2蛋白表達(dá)明顯低于空白對(duì)照組、右美托咪定組和聯(lián)合用藥組(P均0.05),而空白對(duì)照組、右美托咪定組和聯(lián)合用藥組海馬區(qū)PKC、ERK1/2、Bcl-2蛋白表達(dá)比較P均0.05。結(jié)論右美托咪定輔助氯胺酮麻醉對(duì)大鼠海馬區(qū)神經(jīng)細(xì)胞凋亡具有保護(hù)作用,其作用機(jī)制可能與激活PKC-ERK1/2-Bcl-2信號(hào)通路有關(guān)。
[Abstract]:Objective to investigate the protective effect of dexmetomidine-assisted ketamine anesthesia on hippocampal neurons in rats.Methods Thirty-two Sprague-Dawley rats were randomly divided into control group, ketamine group, dexmetomidine group and combined treatment group with 8 rats in each group.The blank control group received intraperitoneal injection of normal saline 50 mL / kg at intervals of 5 min; ketamine group received 70 mg / kg ketamine intraperitoneally and saline 50 mL / kg at intervals of 5 min; dextromidine group received right intraperitoneal injection of normal saline 50 mL / kg; Ketamine group received intraperitoneal injection of normal saline 50 mL / kg; ketamine group received intraperitoneal injection of ketamine 70 mg / kg; interval of 5 minMetoimidine 25 渭 g / kg was subcutaneously injected with normal saline 50 mL / kg at intervals of 5 min, ketamine 70 mg / kg was injected intraperitoneally in the combined treatment group and dexmetidine was injected subcutaneously at intervals of 5 min.Continuous injection for 3 days.Four rats in each group were randomly selected. The respiratory frequency and the time of disappearance of righting reflex were measured in the first injection (n = 4) and the last injection (n = 15 30) (n = 45) and 90 min / t ~ (-1) t ~ (6), respectively.The time of disappearance of righting reflex and complete disappearance of tail reflex was measured by Morris water maze test. The escape latency of 1 to 5 days training in each group was measured.At the end of the last injection of the remaining rats in each group, the apoptotic rate of hippocampal neurons was detected by Tunel method and the expression of Bcl-2 protein was detected by Western blotting.Results compared with the combined treatment group, the vanishing time of the righting reflex in the ketamine group was significantly prolonged, the time of sedation maintenance and the duration of the vanish of the righting reflex were significantly shortened, compared with that in the ketamine group (P < 0.01).The respiratory frequency of ketamine group was significantly higher than that of blank control group.The escape latency of control group, dexmetidine group and combined treatment group was 0.05, and the escape latency of ketamine group was significantly longer than that of blank control group, dexmetomidine group and combined treatment group were significantly longer than that of control group on the 4th day of training (P 0.05).The apoptotic rate of nerve cells in ketamine group was significantly higher than that in blank control group (P 0.05) in dexmetomidine group and combination treatment group, while in blank control group, dexmetomidine group and combined treatment group (P 0.05).The expression of Bcl-2 protein in the hippocampal area of ketamine group was significantly lower than that in the control group. The expression of Bcl-2 protein was significantly lower in the dexmetomidine group and combined treatment group than in the blank control group, the dexmetomidine group and the combined treatment group (P < 0.05), while the expression of Bcl-2 protein in the hippocampal area of the control group, the dexmetomidine group and the combined treatment group was significantly lower than that in the control group (P < 0.05).Conclusion dexmetomidine-assisted ketamine anesthesia has protective effect on neuronal apoptosis in rat hippocampal area, and its mechanism may be related to activation of PKC-ERK1/2-Bcl-2 signaling pathway.
【作者單位】： 山東省醫(yī)學(xué)科學(xué)院附屬醫(yī)院;山東省立醫(yī)院;
【基金】：山東省醫(yī)藥衛(wèi)生科技發(fā)展計(jì)劃(2016WSB01061)
【分類號(hào)】：R614

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