右美托咪啶对七氟醚麻醉患儿麻醉恢复期躁动的影响

Objective To investigate the effect of dexmedetomidine on agitation during recovery from sevoflurane anesthesia in children. Methods Three hundred ASA Ⅰ or Ⅱ children, aged 4-7 yr, weighing 16-30kg, scheduled for elective ear-nose-throat operation under general anesthesia, were randomly divided into 2 groups ( n = 150 each) : control group (group C) and dexmedetomidine group (group D) . Dexmedetomidine 0.5 μg/kg in 20 ml was infused intravenously over 10 min before anesthesia induction in group D, while equal volume of normal Saline was infused in group C. Anesthesia was induced with inhalation of 8 % sevoflurane 5 min after the end of administration . The children were tracheal incubated and mechanically ventilated. Anesthesia was maintained with inhalation of 2 % -3 % sevoflurane. BIS was maintained at 40-60 during operation. The recovery time and agitation within 2 h after operation were recorded. Results There was no significant difference in the recovery time between the two groups ( P > 0.05) . The incidence of agitation was significantly lower in group D than in group C ( P <0.05 ) . Conclusion Dexmedetomidine can reduce the occurrence of agitation during recovery from sevoflurane anesthesia in children.     

右美托咪啶对七氟醚麻醉患儿麻醉恢复期躁动的影响

Objective To investigate the effect of dexmedetomidine on agitation during recovery from sevoflurane anesthesia in children. Methods Three hundred ASA Ⅰ or Ⅱ children, aged 4-7 yr, weighing 16-30kg, scheduled for elective ear-nose-throat operation under general anesthesia, were randomly divided into 2 groups ( n = 150 each) : control group (group C) and dexmedetomidine group (group D) . Dexmedetomidine 0.5 μg/kg in 20 ml was infused intravenously over 10 min before anesthesia induction in group D, while equal volume of normal Saline was infused in group C. Anesthesia was induced with inhalation of 8 % sevoflurane 5 min after the end of administration . The children were tracheal incubated and mechanically ventilated. Anesthesia was maintained with inhalation of 2 % -3 % sevoflurane. BIS was maintained at 40-60 during operation. The recovery time and agitation within 2 h after operation were recorded. Results There was no significant difference in the recovery time between the two groups ( P > 0.05) . The incidence of agitation was significantly lower in group D than in group C ( P <0.05 ) . Conclusion Dexmedetomidine can reduce the occurrence of agitation during recovery from sevoflurane anesthesia in children.     

吸入一氧化碳对大鼠脑死亡致肺损伤的影响

Objective To investigate the effects of carbon monoxide (CO) inhalation on lung injury induced by brain death (BD) in rats. Methods Adult male Wistar rats weighing 250-300 g were used in this study. The animals were anesthetized with intraperitoneal pentobarbital sodium 60 mg/kg, tracheostomized and mechanically ventilated (VT 10 ml/kg, RR 50 bpm, PEEP 2 cm H2O). A balloon-tip catheter was placed in the cranium. Twenty-four rats in which Fogarty catheter was successfully placed in the cranium without complication were randomly divided into 3 groups ( n = 8 each) : group I sham operation (group S) ; group II BD and group Ⅲ BDCO. BD was induced by increase in intracranial pressure produced by inflating the balloon at the tip of the catheter. In group S the balloon of the catheter was not inflated. The animals inhaled 40% O2 for 150 min. In group BD, BD was induced and confirmed at 30 min after inflation of the balloon. Then 40% O2 was inhaled for 120 min. In group BDCO, 40% O2 and 0.025% CO were inhaled for 120 min after BD was confirmed at 30 min after balloon inflation. At the end of the experiment the animals were killed. Arterial blood samples were obtained for blood gas analysis before anesthesia (basline), immediately after confirmation of BD, and at 30, 60, 90 and 120 min of CO inhalation. Blood was collected for determination of plasma TNF-α, IL-6 and IL-10 concentrations at 120 min of CO inhalation. The lungs were obtained for determination of W/D lung weight ratio, and MPO activity in the lung tissue and microscopic examination. Lung injury scores were calculated. Results PaO2/FiO2 was stable during the 150 min in group S. Brain death significantly decreased PaO2/FiO2 at 30 min after balloon inflation. PaO2/FiO2 was gradually decreasing during the 120 min in group BD. CO inhalation prevented PaO2/FiO2 from decreasing further. W/D lung weight ratio and MPO activity were significantly higher in group BD than in group S and BDCO. The lung injury score (1 = normal, 4= severely injured) and plasma TNF-αα IL-6 and IL-10 concentrations were significantly higher in group BD than in group S. CO inhalation ameliorated the BD-induced lung injury and attenuated the increase in plasma TNF-a and IL-6 concentration. Plasma IL-10 concentration was significantly higher in group BDCO than in group BD. Conclusion CO inhalation can ameliorate acute lung injury induced by BD through decreasing the local and systemic inflammatory response.     

吸入一氧化碳对大鼠脑死亡致肺损伤的影响

Objective To investigate the effects of carbon monoxide (CO) inhalation on lung injury induced by brain death (BD) in rats. Methods Adult male Wistar rats weighing 250-300 g were used in this study. The animals were anesthetized with intraperitoneal pentobarbital sodium 60 mg/kg, tracheostomized and mechanically ventilated (VT 10 ml/kg, RR 50 bpm, PEEP 2 cm H2O). A balloon-tip catheter was placed in the cranium. Twenty-four rats in which Fogarty catheter was successfully placed in the cranium without complication were randomly divided into 3 groups ( n = 8 each) : group I sham operation (group S) ; group II BD and group Ⅲ BDCO. BD was induced by increase in intracranial pressure produced by inflating the balloon at the tip of the catheter. In group S the balloon of the catheter was not inflated. The animals inhaled 40% O2 for 150 min. In group BD, BD was induced and confirmed at 30 min after inflation of the balloon. Then 40% O2 was inhaled for 120 min. In group BDCO, 40% O2 and 0.025% CO were inhaled for 120 min after BD was confirmed at 30 min after balloon inflation. At the end of the experiment the animals were killed. Arterial blood samples were obtained for blood gas analysis before anesthesia (basline), immediately after confirmation of BD, and at 30, 60, 90 and 120 min of CO inhalation. Blood was collected for determination of plasma TNF-α, IL-6 and IL-10 concentrations at 120 min of CO inhalation. The lungs were obtained for determination of W/D lung weight ratio, and MPO activity in the lung tissue and microscopic examination. Lung injury scores were calculated. Results PaO2/FiO2 was stable during the 150 min in group S. Brain death significantly decreased PaO2/FiO2 at 30 min after balloon inflation. PaO2/FiO2 was gradually decreasing during the 120 min in group BD. CO inhalation prevented PaO2/FiO2 from decreasing further. W/D lung weight ratio and MPO activity were significantly higher in group BD than in group S and BDCO. The lung injury score (1 = normal, 4= severely injured) and plasma TNF-αα IL-6 and IL-10 concentrations were significantly higher in group BD than in group S. CO inhalation ameliorated the BD-induced lung injury and attenuated the increase in plasma TNF-a and IL-6 concentration. Plasma IL-10 concentration was significantly higher in group BDCO than in group BD. Conclusion CO inhalation can ameliorate acute lung injury induced by BD through decreasing the local and systemic inflammatory response.     

吸入一氧化碳对大鼠脑死亡致肺损伤的影响

Objective To investigate the effects of carbon monoxide (CO) inhalation on lung injury induced by brain death (BD) in rats. Methods Adult male Wistar rats weighing 250-300 g were used in this study. The animals were anesthetized with intraperitoneal pentobarbital sodium 60 mg/kg, tracheostomized and mechanically ventilated (VT 10 ml/kg, RR 50 bpm, PEEP 2 cm H2O). A balloon-tip catheter was placed in the cranium. Twenty-four rats in which Fogarty catheter was successfully placed in the cranium without complication were randomly divided into 3 groups ( n = 8 each) : group I sham operation (group S) ; group II BD and group Ⅲ BDCO. BD was induced by increase in intracranial pressure produced by inflating the balloon at the tip of the catheter. In group S the balloon of the catheter was not inflated. The animals inhaled 40% O2 for 150 min. In group BD, BD was induced and confirmed at 30 min after inflation of the balloon. Then 40% O2 was inhaled for 120 min. In group BDCO, 40% O2 and 0.025% CO were inhaled for 120 min after BD was confirmed at 30 min after balloon inflation. At the end of the experiment the animals were killed. Arterial blood samples were obtained for blood gas analysis before anesthesia (basline), immediately after confirmation of BD, and at 30, 60, 90 and 120 min of CO inhalation. Blood was collected for determination of plasma TNF-α, IL-6 and IL-10 concentrations at 120 min of CO inhalation. The lungs were obtained for determination of W/D lung weight ratio, and MPO activity in the lung tissue and microscopic examination. Lung injury scores were calculated. Results PaO2/FiO2 was stable during the 150 min in group S. Brain death significantly decreased PaO2/FiO2 at 30 min after balloon inflation. PaO2/FiO2 was gradually decreasing during the 120 min in group BD. CO inhalation prevented PaO2/FiO2 from decreasing further. W/D lung weight ratio and MPO activity were significantly higher in group BD than in group S and BDCO. The lung injury score (1 = normal, 4= severely injured) and plasma TNF-αα IL-6 and IL-10 concentrations were significantly higher in group BD than in group S. CO inhalation ameliorated the BD-induced lung injury and attenuated the increase in plasma TNF-a and IL-6 concentration. Plasma IL-10 concentration was significantly higher in group BDCO than in group BD. Conclusion CO inhalation can ameliorate acute lung injury induced by BD through decreasing the local and systemic inflammatory response.     

吸入一氧化碳对大鼠脑死亡致肺损伤的影响

Objective To investigate the effects of carbon monoxide (CO) inhalation on lung injury induced by brain death (BD) in rats. Methods Adult male Wistar rats weighing 250-300 g were used in this study. The animals were anesthetized with intraperitoneal pentobarbital sodium 60 mg/kg, tracheostomized and mechanically ventilated (VT 10 ml/kg, RR 50 bpm, PEEP 2 cm H2O). A balloon-tip catheter was placed in the cranium. Twenty-four rats in which Fogarty catheter was successfully placed in the cranium without complication were randomly divided into 3 groups ( n = 8 each) : group I sham operation (group S) ; group II BD and group Ⅲ BDCO. BD was induced by increase in intracranial pressure produced by inflating the balloon at the tip of the catheter. In group S the balloon of the catheter was not inflated. The animals inhaled 40% O2 for 150 min. In group BD, BD was induced and confirmed at 30 min after inflation of the balloon. Then 40% O2 was inhaled for 120 min. In group BDCO, 40% O2 and 0.025% CO were inhaled for 120 min after BD was confirmed at 30 min after balloon inflation. At the end of the experiment the animals were killed. Arterial blood samples were obtained for blood gas analysis before anesthesia (basline), immediately after confirmation of BD, and at 30, 60, 90 and 120 min of CO inhalation. Blood was collected for determination of plasma TNF-α, IL-6 and IL-10 concentrations at 120 min of CO inhalation. The lungs were obtained for determination of W/D lung weight ratio, and MPO activity in the lung tissue and microscopic examination. Lung injury scores were calculated. Results PaO2/FiO2 was stable during the 150 min in group S. Brain death significantly decreased PaO2/FiO2 at 30 min after balloon inflation. PaO2/FiO2 was gradually decreasing during the 120 min in group BD. CO inhalation prevented PaO2/FiO2 from decreasing further. W/D lung weight ratio and MPO activity were significantly higher in group BD than in group S and BDCO. The lung injury score (1 = normal, 4= severely injured) and plasma TNF-αα IL-6 and IL-10 concentrations were significantly higher in group BD than in group S. CO inhalation ameliorated the BD-induced lung injury and attenuated the increase in plasma TNF-a and IL-6 concentration. Plasma IL-10 concentration was significantly higher in group BDCO than in group BD. Conclusion CO inhalation can ameliorate acute lung injury induced by BD through decreasing the local and systemic inflammatory response.     

七氟醚预先给药对大鼠肾脏缺血再灌注时细胞凋亡的影响

目的 探讨七氟醚预先给药对大鼠肾脏缺血再灌注时细胞凋亡的影响.方法 健康清洁级雄性SD大鼠30只,体重220～260 g,采用随机数字表法,将大鼠随机分为3组(n=10):对照组(C组)、缺血再灌注组(I/R组)、七氟醚组(S组).I/R组和S组采用夹闭左肾蒂45 min后恢复再灌注的方法 建立肾脏缺血再灌注模型,C组腹部正中切口,右肾切除,左肾蒂游离后,缝合腹腔;S组模型制备前30 min开始吸入2.2%七氟醚和氧气的混合气体至再灌注3 h.于再灌注3 h时采集下腔静脉血样5 ml,测定血清尿素氮(BUN)、肌酐(Cr)浓度,然后取肾组织,光镜下观察肾组织病理学结果,TUNEL法检测细胞凋亡,计算细胞凋亡指数,采用RT-PCR和Western blot法测定血红素氧合酶-1(HO-1)mRNA及蛋白表达水平.结果 与C组比较,I/R组和S组血清BUN、Cr浓度、肾脏近曲小管坏死程度、细胞凋亡指数升高,HO-1 mRNA和蛋白表达上调(P＜0.05);与I/R组比较,S组血清BUN、Cr浓度、细胞凋亡指数、肾脏近曲小管坏死程度降低,HO-1 mRNA表达上调(P＜0.05).结论 七氟醚预先给药可通过抑制细胞凋亡而减轻大鼠肾脏缺血再灌注损伤,其抑制细胞凋亡作用可能与HO-1 mRNA表达上调有关.

Abstract：

Objective To investigate the effects of sevoflurane pretreatment on renal ischemia-reperfusion (I/R)-induced apoptosis in kidney in rats. Methods Thirty pathogen-free male SD rats weighing 220-260 g were randomized into 3 groups (n=10 each):group control (group C);group I/R and group sevoflurane(group S). Renal I/R was induced by clamping the left renal pedicle for 45 min in I/R and S groups. In group S inhalation of 2.2% sevoflurane in O2 was started at 30 min before operation and maintained throughout the experiment.Venous blood samples were taken at 3 h of reperfusion for determination of serum BUN and Cr concentrations. The animals were then sacrificed and the left kidneys were removed for microscopic examination, detection of apoptosis(by TUNEL)and determination of heme oxygenase-1(HO-1) mRNA and protein expression (by RT-PCR and Western blot).Results Renal I/R significantly increased serum BUN and Cr concentrations, apoptotic index(percentage of apoptotic cells) and the severity of necrosis of renal proximal convoluted tubules (0=normal,4=necrosis of whole segment of proximal convoluted tubules).Sevoflurane inhalation attenuated the I/R-induced changes mentioned above.HO-1 mRNA and protein expression was up-regulated by I/R and HO-1 mRNA expression was further up-regulated by sevoflurane inhalation.Conclusion Sevoflurane pretreatment can protect kidney against I/R injury by attenuating cell apoptosis.Up-regulation of HO-1 mRNA expression may be involved in the mechanism.     

吸入一氧化碳对大鼠脑死亡致肺损伤的影响

Objective To investigate the effects of carbon monoxide (CO) inhalation on lung injury induced by brain death (BD) in rats. Methods Adult male Wistar rats weighing 250-300 g were used in this study. The animals were anesthetized with intraperitoneal pentobarbital sodium 60 mg/kg, tracheostomized and mechanically ventilated (VT 10 ml/kg, RR 50 bpm, PEEP 2 cm H2O). A balloon-tip catheter was placed in the cranium. Twenty-four rats in which Fogarty catheter was successfully placed in the cranium without complication were randomly divided into 3 groups ( n = 8 each) : group I sham operation (group S) ; group II BD and group Ⅲ BDCO. BD was induced by increase in intracranial pressure produced by inflating the balloon at the tip of the catheter. In group S the balloon of the catheter was not inflated. The animals inhaled 40% O2 for 150 min. In group BD, BD was induced and confirmed at 30 min after inflation of the balloon. Then 40% O2 was inhaled for 120 min. In group BDCO, 40% O2 and 0.025% CO were inhaled for 120 min after BD was confirmed at 30 min after balloon inflation. At the end of the experiment the animals were killed. Arterial blood samples were obtained for blood gas analysis before anesthesia (basline), immediately after confirmation of BD, and at 30, 60, 90 and 120 min of CO inhalation. Blood was collected for determination of plasma TNF-α, IL-6 and IL-10 concentrations at 120 min of CO inhalation. The lungs were obtained for determination of W/D lung weight ratio, and MPO activity in the lung tissue and microscopic examination. Lung injury scores were calculated. Results PaO2/FiO2 was stable during the 150 min in group S. Brain death significantly decreased PaO2/FiO2 at 30 min after balloon inflation. PaO2/FiO2 was gradually decreasing during the 120 min in group BD. CO inhalation prevented PaO2/FiO2 from decreasing further. W/D lung weight ratio and MPO activity were significantly higher in group BD than in group S and BDCO. The lung injury score (1 = normal, 4= severely injured) and plasma TNF-αα IL-6 and IL-10 concentrations were significantly higher in group BD than in group S. CO inhalation ameliorated the BD-induced lung injury and attenuated the increase in plasma TNF-a and IL-6 concentration. Plasma IL-10 concentration was significantly higher in group BDCO than in group BD. Conclusion CO inhalation can ameliorate acute lung injury induced by BD through decreasing the local and systemic inflammatory response.     

吸入一氧化碳对大鼠脑死亡致肺损伤的影响

Objective To investigate the effects of carbon monoxide (CO) inhalation on lung injury induced by brain death (BD) in rats. Methods Adult male Wistar rats weighing 250-300 g were used in this study. The animals were anesthetized with intraperitoneal pentobarbital sodium 60 mg/kg, tracheostomized and mechanically ventilated (VT 10 ml/kg, RR 50 bpm, PEEP 2 cm H2O). A balloon-tip catheter was placed in the cranium. Twenty-four rats in which Fogarty catheter was successfully placed in the cranium without complication were randomly divided into 3 groups ( n = 8 each) : group I sham operation (group S) ; group II BD and group Ⅲ BDCO. BD was induced by increase in intracranial pressure produced by inflating the balloon at the tip of the catheter. In group S the balloon of the catheter was not inflated. The animals inhaled 40% O2 for 150 min. In group BD, BD was induced and confirmed at 30 min after inflation of the balloon. Then 40% O2 was inhaled for 120 min. In group BDCO, 40% O2 and 0.025% CO were inhaled for 120 min after BD was confirmed at 30 min after balloon inflation. At the end of the experiment the animals were killed. Arterial blood samples were obtained for blood gas analysis before anesthesia (basline), immediately after confirmation of BD, and at 30, 60, 90 and 120 min of CO inhalation. Blood was collected for determination of plasma TNF-α, IL-6 and IL-10 concentrations at 120 min of CO inhalation. The lungs were obtained for determination of W/D lung weight ratio, and MPO activity in the lung tissue and microscopic examination. Lung injury scores were calculated. Results PaO2/FiO2 was stable during the 150 min in group S. Brain death significantly decreased PaO2/FiO2 at 30 min after balloon inflation. PaO2/FiO2 was gradually decreasing during the 120 min in group BD. CO inhalation prevented PaO2/FiO2 from decreasing further. W/D lung weight ratio and MPO activity were significantly higher in group BD than in group S and BDCO. The lung injury score (1 = normal, 4= severely injured) and plasma TNF-αα IL-6 and IL-10 concentrations were significantly higher in group BD than in group S. CO inhalation ameliorated the BD-induced lung injury and attenuated the increase in plasma TNF-a and IL-6 concentration. Plasma IL-10 concentration was significantly higher in group BDCO than in group BD. Conclusion CO inhalation can ameliorate acute lung injury induced by BD through decreasing the local and systemic inflammatory response.     

吸入一氧化碳对大鼠脑死亡致肺损伤的影响

Objective To investigate the effects of carbon monoxide (CO) inhalation on lung injury induced by brain death (BD) in rats. Methods Adult male Wistar rats weighing 250-300 g were used in this study. The animals were anesthetized with intraperitoneal pentobarbital sodium 60 mg/kg, tracheostomized and mechanically ventilated (VT 10 ml/kg, RR 50 bpm, PEEP 2 cm H2O). A balloon-tip catheter was placed in the cranium. Twenty-four rats in which Fogarty catheter was successfully placed in the cranium without complication were randomly divided into 3 groups ( n = 8 each) : group I sham operation (group S) ; group II BD and group Ⅲ BDCO. BD was induced by increase in intracranial pressure produced by inflating the balloon at the tip of the catheter. In group S the balloon of the catheter was not inflated. The animals inhaled 40% O2 for 150 min. In group BD, BD was induced and confirmed at 30 min after inflation of the balloon. Then 40% O2 was inhaled for 120 min. In group BDCO, 40% O2 and 0.025% CO were inhaled for 120 min after BD was confirmed at 30 min after balloon inflation. At the end of the experiment the animals were killed. Arterial blood samples were obtained for blood gas analysis before anesthesia (basline), immediately after confirmation of BD, and at 30, 60, 90 and 120 min of CO inhalation. Blood was collected for determination of plasma TNF-α, IL-6 and IL-10 concentrations at 120 min of CO inhalation. The lungs were obtained for determination of W/D lung weight ratio, and MPO activity in the lung tissue and microscopic examination. Lung injury scores were calculated. Results PaO2/FiO2 was stable during the 150 min in group S. Brain death significantly decreased PaO2/FiO2 at 30 min after balloon inflation. PaO2/FiO2 was gradually decreasing during the 120 min in group BD. CO inhalation prevented PaO2/FiO2 from decreasing further. W/D lung weight ratio and MPO activity were significantly higher in group BD than in group S and BDCO. The lung injury score (1 = normal, 4= severely injured) and plasma TNF-αα IL-6 and IL-10 concentrations were significantly higher in group BD than in group S. CO inhalation ameliorated the BD-induced lung injury and attenuated the increase in plasma TNF-a and IL-6 concentration. Plasma IL-10 concentration was significantly higher in group BDCO than in group BD. Conclusion CO inhalation can ameliorate acute lung injury induced by BD through decreasing the local and systemic inflammatory response.     

海马内DNA甲基转移酶在七氟醚所致新生大鼠远期认知功能损伤中的作用

目的观察海马内DNA甲基转移酶(DNMTs)在七氟醚所致新生大鼠远期认知功能损伤中的作用。方法出生7d雄性SD大鼠64只,随机均分为四组(n=16):对照组(C组)、七氟醚组(S组)、七氟醚+生理盐水组(SN组)及七氟醚+5-杂氮胞苷组(5-AZA,DNMTs抑制剂,SA组)。C组吸入30%O22h,连续3d;S组、SN组和SA组吸入3%七氟醚+30%O22h,连续3d;SA组在七氟醚吸入前1h时侧脑室注入5-AZA 1mg/kg;SN组则注射等容量生理盐水。4周后,一部分大鼠行旷场实验和Morris水迷宫实验(n=8),另一部分取海马组织(n=8),采用实时荧光定量PCR和Western blot分别检测DNMT1、DNMT3a、DNMT3b的mRNA和蛋白含量。结果旷场实验中,四组大鼠探索路程和中央格停留时间差异无统计学意义。与C组比较,S组在Morris水迷宫实验中逃逸潜伏期明显延长,目标象限探索时间明显缩短,海马内DNMT3a及DNMT3b的mRNA和蛋白含量明显增加(P0.05);与SN组比较,SA组逃逸潜伏期明显缩短,目标象限探索时间明显延长,海马内DNMT3a及DNMT3b的mRNA和蛋白含量明显减少(P0.05);四组海马内DNMT1的mRNA和蛋白含量差异无统计学意义。结论七氟醚可致新生大鼠远期认知功能损伤伴海马内DNMT3a和DNMT3b表达增加;5-AZA可降低海马内DNMT3a及DNMT3b表达,减轻七氟醚所致新生大鼠远期认知功能损伤,表明DNMTs参与了七氟醚所致新生大鼠远期认知功能损伤的过程。     

不同浓度七氟烷对老年大鼠认知功能的影响

目的 探讨不同浓度七氟烷对老年大鼠认知功能的影响.方法 18月龄雄性SD大鼠40只,体重500～650 g,随机分为3组,对照组(C组,n=8)吸入空气,1.5%七氟烷组(S1组,n=16)吸入1.5%七氟烷2 h,3.0%七氟烷组(S2组,n=16)吸入3.0%七氟烷2 h.于吸入七氟烷后1、7 d(T1.2)S1组和S2组随机取8只大鼠,采用Y型迷宫实验行认知功能测试,认知功能测试后12 h时处死大鼠,断头取脑,采用RT-PCR方法测定左侧海马N-甲基-D-天冬氨酸受体2B亚基(NR2B)mRNA表达,采用免疫组化法检测右侧海马NR2B蛋白表达.结果 与C组比较,S2组吸入七氟烷后1 d大鼠认知功能减退,右侧海马NR2B蛋白、左侧海马NR2B mRNA表达上调(P<0.05),S1.组上述指标差异无统计学意义(P0.05).结论 吸入1.5%七氟烷后老年大鼠认知功能无明显变化;吸入3%七氟烷后1 d老年大鼠认知功能减退,可能与其上调海马含2B亚基的NMDA受体表达有关.     

反复吸入七氟醚对老龄大鼠海马组织Apaf-1和Caspase-9 mRNA表达的影响

目的 探讨反复吸入七氟醚对老龄大鼠海马组织凋亡蛋白酶活化因子-1(Apaf-1)及半胱氨酸天冬氨酸蛋白酶-9(Caspase-9)mRNA表达的影响.方法 健康Wistar大鼠30只,月龄22月,体重380～770 g,雌雄各半,随机分为4组:对照组(n=8,Ⅰ组)、2%七氟醚组(n=8,Ⅱ组)、3%七氟醚组(n=8,Ⅲ组)及颈总动脉结扎+2%七氟醚组(n=6,IV组).Ⅰ组不吸入七氟醚,Ⅱ组及Ⅲ组分别吸入2%、3%七氟醚,100 min/d,连续5 d.Ⅳ组结扎左侧颈总动脉,1周后吸入2%七氟醚,100 min/d,连续5 d.停止吸入七氟醚后第1天开始采用Morris水迷宫实验测定大鼠认知功能,4次/d,连续测定5 d(T_(1～5)),记录潜伏期、平台象限活动时间与总游泳时间的百分比(Tp/T)及撤去平台后2 min内的游泳轨迹.水迷宫实验结束后采用RT-PCR法测定海马组织Apaf-1、Caspase-9 mRNA的表达水平.结果 与T_1时比较,Ⅰ组T_(3～5)、Ⅱ组及Ⅲ组T_(2～5)时、Ⅳ组T_(4,5)时潜伏期缩短(P<0.05或0.01);与Ⅰ组比较,Ⅲ组T_1时、Ⅳ组T_(1～5),时潜伏期延长,Ⅲ组及Ⅳ组Tp/T降低,Ⅳ组Caspase-9 mRNA表达上调(P<0.05或0.01).撤去平台后,Ⅱ组大鼠游泳轨迹明显集中在平台象限(Ⅳ象限),Ⅲ组和Ⅳ组大鼠游泳轨迹明显散乱.结论 反复吸入七氟醚可导致老龄大鼠认知功能障碍,其机制与海马组织Apaf-1及Caspase-9 mRNA的表达无关.     

七氟烷后处理对大鼠海马缺血性损伤及胰岛素样生长因子-1表达的影响

目的 观察不同浓度七氟烷后处理对大鼠海马缺血性损伤的保护作用及其对胰岛素样生长因子-1(insulin-like growth factor-1,IGF-1)表达的影响.方法 选取雄性SD大鼠,随机分为6组:假手术组(S)、缺血但无后处理组(C)、吸氧后处理组(O_2)、不同浓度七氟烷后处理组(Sevo1组、Sevo2组、Sevo3组);不同浓度七氟烷后处理组于脑缺血/再灌注即刻给予吸入1.5%(Sevo1组)、2.4%(Sevo2组)、3.0%(Sevo3组)的七氟烷30 min.采用大脑中动脉闭塞(MCAO)改良模型,于再灌注后的24、48、72h对海马进行组织病理学观察及IGF-1 mRNA检测.结果 与S组相比,C组各时间点大鼠海马IGF-1 mRNA的表达增加(P＜0.05)且海马组织出现病理学损伤;与C组相比,Scvo2组、Scvo3组各时间点的海马IGF-1 mRNA表达进一步增加(P＜0.05),且海马组织病理学损伤较轻;Sevo1组与C组相比,海马IGF-1mRNA的表达及病理学损伤无明显差异.结论 较高浓度的七氟烷后处理可以通过上调海马IGF-1及其受体系统而发挥中枢神经保护作用.     

反复吸入七氟烷对老年大鼠认知功能的影响

目的 评价反复吸入七氟烷对老年大鼠认知功能的影响.方法 健康Wistar大鼠24只,月龄18月,体重270-450 g,雌雄各半,随机分为3组(n=8):对照组(C组)、2%七氟烷组(S1组)和3%七氟烷组(S2组).C组不吸入七氟烷;S1和S2组分别吸入2%、3%七氟烷,100 min/d,连续5d.于干预结束后1-6d(T1-6)时进行水迷宫实验,记录T1-5时游泳时间和游泳距离及T6时第4象限探索时间和游泳距离.于最后1次水迷宫实验结束后60 min处死大鼠,取海马组织,采用RT-PCR法测定海马N-甲基肌天冬氨酸受体(NMDAR)、NR1和NR2B mRNA的表达.结果 与C组比较,S1组T1时游泳时间和游泳距离延长.T6时第4象限探索时间缩短,NMDAR mRNA表达上调(P<0.05),NRI和NR2B mRNA的表达差异无统计学意义(P<0.05).结论 反复吸入2%七氟烷不会导致老年大鼠认知功能减退;而反复吸入3%七氟烷可导致一过性认知功能减退.     

七氟醚暴露致新生大鼠未成熟脑损伤的研究

目的探讨七氟醚早期暴露对新生大鼠脑发育的影响。方法选取新生6日龄SD大鼠80只,随机分为四组,每组20只,分别为空白对照组(C组),1%七氟醚暴露2 h组(Sev1组),2%七氟醚暴露2 h组(Sev2组),4%七氟醚暴露2 h组(Sev3组);七氟醚暴露组分别置于1%、2%、4%七氟醚中每天暴露2 h,连续3 d;出生后第9天采用0.5%戊巴比妥钠麻醉后处死新生大鼠取出脑组织;采用电子天平秤检测各组大鼠在出生后6、9、15、28 d体重和脑重的变化;采用荧光定量PCR法(RT-PCR)检测Cx30、IL-6及BDNF基因mRNA表达量;采用免疫荧光法检测GFP蛋白含量;出生后28 d Morris水迷宫评价新生大鼠学习记忆能力。结果与C组比较,Sev1、Sev2和Sev3组新生大鼠体质量和脑质量均有所减轻,且随着日期延长这种减轻更为明显,Cx30 mRNA和BDNF mRNA表达量明显降低,IL-6mRNA表达量明显升高(P0.05),GFP细胞数量明显减少(P0.05);与Sev1组比较,Sev2和Sev3组新生大鼠体质量和脑质量均明显减轻,GFP数量明显减少(P0.05);与C组比较,Sev1、Sev2和Sev3组逃避潜伏期和游动距离均明显延长(P0.05),目标象限停留时间明显缩短(P0.05),穿越虚拟平台次数明显减少(P0.05)。结论新生大鼠接受七氟醚暴露可致未成熟脑损伤及远期学习记忆能力下降,且这种脑损伤程度与七氟醚浓度呈正相关;其机制可能与其脑内Cx30、BDNF基因表达水平改变有关。     

七氟烷不同吸入浓度与时间对新生大鼠认知功能及海马脑源性神经营养因子表达的远期影响

目的 评价七氟烷不同吸入浓度与时间对新生大鼠认知功能和海马脑源性神经营养因子(brain derived neurotrophic factor,BDNF)表达的远期影响.方法 7d龄SD大鼠采用随机数字表法随机分为4组(每组20只):空白对照组(C组)、5.1％七氟烷1.3 h组(S组)、3.4％七氟烷2h组(M组)...     

异氟醚对大鼠海马高级糖基化终末产物受体表达的影响

目的 探讨异氟醚对大鼠海马高级糖基化终末产物受体(RAGE)表达的影响.方法 雄性老龄SD大鼠45只,月龄24月;雄性成年SD大鼠45只,月龄4月,分为老龄组和成年组(n=45),每组再分为3个亚组(n=15):老龄对照组(OC组)和成年对照组(AC组)吸入含30%氧气的空氧混合气体;老龄单次吸入异氟醚组(OS组)和成年单次吸入异氟醚组(AS组)吸入1.5%异氟醚2 h;老龄多次吸入异氟醚组(OR组)和成年多次吸入异氟醚组(AR组)吸入1.5%异氟醚3次,2 h/次,每天1次.吸入异氟醚后1 d各组随机取8只大鼠行Morris水迷宫实验测定认知功能,余大鼠处死取海马,采用RT-PCR法检测RAGE mRNA的表达水平,免疫组织化学法检测RAGE蛋白的表达水平.结果 与OC组比较,OS组和OR组认知功能减退,海马RAGE mRNA及其蛋白的表达上调(P＜0.05);与AC组比较,AS组和AR组认知功能减退,AR组海马RAGE mRNA及其蛋白的表达上调(P＜0.05);与OS组比较,OR组认知功能减退,海马RAGE mRNA表达上调(P＜0.05);与AS组比较,AR组认知功能减退,海马RAGE mRNA及其蛋白的表达上调(P＜0.05).结论 异氟醚可导致老龄和成年大鼠认知功能降低,尤其对老龄大鼠影响明显,可能与其上调海马RAGE表达有关.     

七氟醚对不同性别大鼠海马神经元p-CREB1表达的影响

目的 评价七氟醚对不同性别大鼠海马神经元磷酸化cAMP反应元件结合蛋白1(p-CREB1)表达的影响.方法 健康成年雌性SD大鼠30只,3月龄,体重180～220 g,采用随机数字表法,将大鼠随机分为2组(n＝15):对照组(Fc组)和七氟醚组(Fs组);健康成年雄性SD大鼠28只,3月龄,体重380-440 g,采用随机数字表法,将大鼠随机分为2组(n＝14):对照组(Mc组)和七氟醚组(Ms组).Fc组和Mc组吸入95％氧气(流量4 L/min)2 h,Fs组和Ms组吸入3％七氟醚2h.于停止吸入七氟醚后2d时行避暗实验;于停止吸入七氟醚后3～7d时行Morris水迷宫实验,第7天认知功能测定结束后处死大鼠,取脑组织,剥离海马,采用Western blot法检测海马组织p-CREB1及Bcl-2、caspase-8的表达水平.结果 与Fc组比较,Fs组停止吸入七氟醚后3d时逃避潜伏期延长,游泳总路程增加,海马组织p-CREB1和Bcl-2表达下调,caspase-8表达上调(P<0.05);与Mc组比较,Ms组停止吸入七氟醚后3～6d时逃避潜伏期延长,游泳总路程增加,海马组织p-CREB1和Bcl-2表达下调,caspase-8表达上调(P<0.05);与Fs组比较,Ms组停止吸入七氟醚后4～6d时逃避潜伏期延长,游泳总路程增加,海马组织p-CREB1和Bcl-2表达下调(P<0.05).结论 七氟醚可通过抑制海马神经元CREB1蛋白磷酸化,上调caspase-8蛋白表达,下调Bcl-2蛋白表达,促进神经元凋亡,导致大鼠认知功能减退,且对雄性大鼠的效应更明显.     

反复吸入七氟烷对幼年大鼠认知功能的影响

目的 评价反复吸入七氟烷对幼年大鼠认知功能的影响.方法 健康雄性SD大鼠108只,25～35日龄,体重90～100 g,随机分为6组(n=18),C1组、C2组和C3组每天同一时间吸入纯氧0.5 L/min,1 h/次,分别吸入1、3、5 d;S1组、S2组和S3组每天同一时间吸入2.3%七氟烷及纯氧0.5 L/min,1 h/次,分别吸1、3、5 d.干预结束后7 d,各组随机取10只大鼠进行水迷宫实验,记录达标所需训练次数、逃避潜伏期及进入盲端次数;其余8只记录神经电生理强直刺激后群峰电位(PS)振幅,计算长时程增强(LTP)诱发成功率.结果 各组大鼠水迷宫实验达标所需训练次数、逃避潜伏期及进入盲端次数差异无统计学意义(P>0.05).与C3组比较,S3组LTP诱发成功率降低(P<0.05);C1组与S1组比较、C2组与S2组比较差异均无统计学意义(P>0.05).结论 反复吸入七氟烷虽可抑制幼年大鼠LTP形成,但抑制程度较轻,对认知功能无明显影响.