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[目的]观察麻醉苏醒室低氧血症病人不同给氧方式的效果。[方法]将麻醉苏醒室发生低氧血症的60例病人随机分为观察组和对照组各30例,对照组采取双孔鼻导管吸氧,观察组采取非重复式呼吸面罩吸氧。观察两组病人入苏醒室后即刻(T1)、入苏醒室30min(T2)2个时间点的二氧化碳分压(PaCO_2)、氧分压(PaO_2)、pH值、动脉血氧饱和度(SaO_2);调查两组病人对T2时间点的鼻腔干燥不适、吸氧异味、恶心呕吐及胸闷不适的满意度;观察病人在T1、T2时间点平均动脉压(MAP)、心率(HR)、脉搏血氧饱和度(SPO_2)。[结果]两组病人组内吸氧前后PaO_2、SPO_2比较,吸氧后T2时间点PaO_2、SPO_2比较,差异有统计学意义(P0.05);观察组在T2时间点心率减慢程度显著高于对照组,差异有统计学意义(P0.05);观察组病人鼻腔干燥不适、吸氧异味满意度高于对照组,差异有统计学意义(P0.05)。[结论]麻醉苏醒室低氧血症病人采取非重复式呼吸面罩吸氧能有效改善氧分压和生命体征,利于术后康复。 相似文献
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目的 评价氯化锂(LiCl)预先给药对异氟醚麻醉诱发老龄大鼠认知功能障碍及海马炎性反应的影响.方法 老龄雄性SD大鼠80只,20月龄,体重350 ~400g,采用随机数字表法,将大鼠随机分为4组(n=20):对照组(C组)吸入30%O2-70% N26h;异氟醚麻醉组(I组)吸入1.4%异氟醚6h,以30%O2-70%N2作为载气;LiCl+异氟醚麻醉组(L+I组)腹腔注射LiC1 100 mg/kg,1次/d,连续3d,第4d行异氟醚麻醉;LiCl组(L组)腹腔注射LiCl 100 mg/kg,1次/d,连续3d,第4d吸入30% O2-70% N26h.麻醉结束即刻行动脉血气分析,麻醉结束后24h取海马组织,采用Western blot法测定海马糖原合成酶激酶-3β(GSK-3β)和核因子κB第310赖氨酸乙酰化蛋白[acetyl-NF-κB (Lys310)]的表达,采用实时定量PCR和ELISA法分别检测海马TNF-α、IL1β和IL-6的mRNA表达及其含量;麻醉结束后第2d评估认知功能.结果 与C组比较,I组GSK-3β和acetyl-NF-κB (Lys310)表达上调,TNF-α、IL-1β及IL-6含量及其mRNA表达水平升高,逃避潜伏期延长,探索时间缩短(P<0.05),L+I组和L组上述指标差异无统计学意义(P>0.05);与I组比较,L+I组GSK-3β、acetyl-NF-κB (Lys310)表达下调,TNF-α、IL-1β、IL-6含量及其mRNA表达水平降低,逃避潜伏期缩短,探索时间延长(P<0.05).结论 氯化锂预先给药可改善异氟醚麻醉诱发老龄大鼠认知功能障碍,其机制与抑制海马炎性反应有关. 相似文献
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目的探讨异氟醚麻醉对新生大鼠海马神经元N-甲基-D-天冬氨酸(NMDA)受体亚基及凋亡的影响。方法新生1d的SD大鼠36只,雌雄不拘,取海马组织进行原代培养。采用随机数字表法将培养海马神经元5d的培养皿随机分为三组:对照组(C组)、异氟醚组(I组)和AP5+异氟醚组(A组),每组12只。I组和A组培养的海马神经元放置在密闭箱中,吸入1.5%异氟醚和纯氧,吸入时间6h,C组不做任何处理。于异氟醚麻醉结束后2、4、6、24h(C组于相应时点),提取海马神经元总mRNA和总蛋白,采用RT-PCR法测定NR2A mRNA、NR2BmRNA和caspase-3mRNA的表达量,采用Westen blot法测定caspase-3蛋白含量。结果与C组比较,异氟醚麻醉结束后2、4和6hI组海马神经元NR2AmRNA和NR2BmRNA的表达量明显上调(P0.05)。与C组和A组比较,I组异氟醚麻醉结束后2、4和6h海马神经元caspase-3mRNA的表达量、异氟醚麻醉后4和6h海马caspase-3蛋白含量明显升高(P0.05)。结论吸入1.5%异氟醚可能通过上调新生大鼠海马神经元NMDA受体导致发育神经元凋亡,阻断NMDA受体可以预防异氟醚导致的发育期海马神经元凋亡。 相似文献
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目的 观察米诺环素对异氟醚诱导的发育期大鼠神经元毒性的保护作用.方法 取新生SD大鼠皮层,随机分为四组,每组10只.正常对照组(C组)神经元在37℃空气处理6h,异氟醚麻醉组(A组)神经元在37℃下用1.5%异氟醚处理6h,米诺环素1μmol/L组(M1组)和米诺环素10μmol/L组(M2组)神经元分别在异氟醚处理10 min前加入米诺环素1μmol/L、10μmol/L.相差显微镜下观察四组神经元形态,TUNEL法检测神经元凋亡,MTT法检测神经元活性.结果 A组神经元胞体肿胀、变形且与M1组神经元形态接近;M2组神经元形态改变不明显且与C组相近.MTT结果 显示,与C组、M2组相比,A组、M1组神经元活性显著降低(P<0.05),凋亡神经元数目显著增多(P<0.05).结论 米诺环素能减轻异氟醚诱导的发育期大鼠神经元毒性,具有保护作用. 相似文献
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This study examined the effects of clinically relevant concentrations of isoflurane on the amplitude of NMDA receptor current (INMDA) and the expression of cytochrome C in cultured developing rat hippo... 相似文献
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目的 探讨嗅物位在全身麻醉气管插管手术患者中的应用效果.方法 选择我院腹腔镜胆囊切除全身麻醉手术患者140例,采用随机数字表法分为观察组和对照组各70例.对照组患者采取常规去枕仰卧位,观察组采取嗅物位,观察比较2组手术患者的气管插管时间、Cormack-Lehane喉头分级、并发症及生命体征.结果 观察组气管插管时间及并发症发生率低于对照组(P<0.05),观察组首次气管插管成功率高于对照组(P<0.05),Cormack-Lehane喉头分级优于对照组(P<0.05),观察组气管插管后心率和平均动脉压优于对照组(P<0.05).结论 手术患者气管插管时采用嗅物位,能提高首次气管插管成功率,降低恶心呕吐、咽喉部不适发生,并维持血流动力学稳定. 相似文献
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临床常用吸入性全身麻醉药异氟烷、七氟烷和地氟烷等均能增强机体对外源性氨酪酸(GABA)的电反应,通过GABAA发挥生物学效应。而在发育期神经元电生理功能具有阶段特异性:GABAA受体介导的氯离子外流引起神经元去极化;α氨基羟甲基唑丙酸受体尚无完整功能,N甲-基-D-天冬氨酸受体的激活依赖GABAA受体,在神经元突触形成方面起着重要的作用。此外,氯离子引导的除极还可以激活细胞膜上电压依赖性钙通道引起钙内流。发育期神经元电生理特点使其在生长发育过程中容易受到吸入性全身麻醉药的影响。 相似文献
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This study investigated the role of glycogen synthase kinase-3β (GSK-3β) in isoflurane-induced neuroinflammation and cognitive dysfunction in aged rats.The hippocampi were dissected from aged rats which had been intraperitoneally administered lithium chloride (LiCl,100 mg/kg) and then exposed to 1.4% isoflurane for 6 h.The expression of GSK-3β was detected by Western blotting.The mRNA and protein expression levels of tumor necrosis factor (TNF)-α,interleukin (IL)-1β and IL-6 were measured by real-time PCR and enzyme-linked immunosorbent assay (ELISA),respectively.Morris water maze was employed to detect spatial memory ability of rats.The results revealed that the level of GSK-3β was upregulated after isofurane exposure.Real-time PCR analysis demonstrated that isoflurane anesthesia increased mRNA levels of TNF-α,IL-1β and IL-6,which was consistent with the ELISA results.However,these changes were reversed by prophylactic LiCl,a non-selective inhibitor of GSK-3β.Additionally,we discovered that LiCl alleviated isoflurane-induced cognitive impairment in aged rats.Furthermore,the role of GSK-3β in isoflurae-induced neuroinflammation and cognitive dysfunction was associated with acetylation of NF-κB p65 (Lys310).In conclusion,these results suggested that GSK-3β is associated with isoflurane-induced upregulation of proinflammatory cytokines and cognitive disorder in aged rats. 相似文献
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目的 探讨异氟醚麻醉对新生大鼠海马激活肌细胞增强因子2(MEF2)信号通路的影响.方法 取出生5 d的SD大鼠24只,雌雄不拘,体重10~13 g,采用随机数字表法,将大鼠随机分为2组(n=12):对照组(C组)和异氟醚组(I组).I组大鼠放置在密闭箱中,吸人1.5%异氟醚和纯氧,吸入时间6 h,C组不做任何处理.于异氟醚麻醉2、4、6 h和麻醉结束后24 h(T1-4)时(C组于相应时点)分别取3只大鼠,断头处死,取海马组织,采用RT-PCR法测定MEF2mRNA、synGAPⅠ mRNA和Arc mRNA及突触素Ⅰ mRNA的表达水平,采用Westrn blot法测定突触素Ⅰ蛋白的表达水平.结果 与C组比较,I组T1-3时海马MEF2mRNA、synGAP Ⅰ mRNA、Arc mRNA和突触素Ⅰ mRNA、T2-4时海马突触素Ⅰ蛋白表达水平均上调(P<0.05).结论 吸入麻醉浓度的异氟醚可能通过激活新生大鼠海马MEF2信号通路从而影响发育期突触的形成.Abstract: Objective To investigate the effects of isoflurane anenthesia on myocyte enhancer factor 2(MEF2) signaling pathway in neonatal rat hippocampus. Methods Twenty-four 5-day-old SD rats of both sexes,weighing 10-13 g, were randomly divided into 2 groups ( n = 12 each): control group (group C) and isoflurane group (group I). In group I, 1.5% isoflurane in 100% O2 was inhaled for 6 h. Group C received no treatment.Three rata in each group were sacrificed at 2, 4, 6 h of isoflurane anenthesia and 24 h after isoflurane anenthesia (T1-4), and the hippocampi removed for determination of MEF2 mRNA, synGAP Ⅰ mRNA, Arc mRNA and synapsinⅠ mRNA expression (by PT-PCR) and synapsin Ⅰ protein expression (by Western blot).Results Compared with group C, the expression of MEF2 mRNA, synGAP Ⅰ mRNA, Arc mRNA and synapsin Ⅰ mRNA at T1-3 and synapsin Ⅰ protein at T2-4 was up-regulated in group I ( P < 0.05). Conclusion Inhalation of anaesthetic concentration of isoflurane may affect synapse formation during the development of central nervous system by actirating hippocampal MEF2 signaling pathways in neonatal rats. 相似文献