TRPA1激动剂桂皮醛防止高糖介导的心肌细胞氧化应激损伤

目的 探讨桂皮醛对高糖介导的心肌细胞氧化应激损伤的作用及机制。方法 大鼠心肌细胞（H9C2）以高糖培养基（33 mmol/L D-葡萄糖）培养,以低糖培养基（5.5 mmol/L D-葡萄糖）作为对照。首先利用Western blot和免疫组织化学证实瞬时受体电位通道A1亚型（TRPA1）在H9C2心肌细胞中的表达;在此基础上分别利用线粒体超氧化物荧光探针（mitoSOX）及TUNEL细胞凋亡试剂盒观察桂皮醛对高糖环境下H9C2细胞线粒体活性氧(ROS)水平以及细胞凋亡的影响,以Western blot法观察Nrf2和TRPA1的表达;利用荧光定量PCR观察TRPA1及Nrf2 mRNA水平。结果 TRPA1在H9C2细胞中有表达,桂皮醛可显著抑制高糖介导线粒体ROS生成（P<0.01）,并可减少心肌细胞的凋亡（P<0.01）,而上述作用可被TRPA1的阻断剂HC 030031所阻断。桂皮醛可上调TRPA1、Nrf2的蛋白及mRNA表达（P<0.01）,而通过HC 030031抑制TRPA1可显著减弱桂皮醛的上述作用（P<0.01）。结论 桂皮醛可防止高糖介导的心肌细胞氧化应激损伤,而该作用可能与其激活TRPA1,上调Nrf2有关。     

缺血预处理-后处理对大鼠肠缺血再灌注损伤的影响

Objective To evaluate the effects of ischemic preconditioning-postconditioning on the intestinal ischemia-reperfusion (IR) injury in rats. Methods Forty healthy male SD weighing 225-275 g were randomly assigned into 5 groups ( n = 8 each): group I sham operation (group S) ; group II intestinal IR (group IIR); group Ⅲ ischemic preconditioning (group Ipr); group IV ischemic postconditioning (group Ipo); group V Ipr+ Ipo. The rats were anesthetized with intraperitonel 20% urethane 5 ml/kg. Superior mesenteric artery (SMA) was occluded for 60 min followed by 60 min reperfusion. In group S, SMA was isolated but not occluded. In group Ipr, SMA was occluded for 10 min followed by 10 min reperfusion, and the rest procedures were performed using the method described in group IIR. In group Ipo, 60 min ischemia was followed by three 30 s episodes of ischemia at 30 s intervals for reperfusion. In group Ipr+ Ipo, Ipr was performed followed by Ipo and the procedures were performed using the methods described in group Ipr and Ipo. The animals were killed at 60 min of reperfusion. The intestinal tissues were immediately removed for determination of MDA content, SOD and MPO activities and the degree of damage to intestinal mucous membrane was scored according to Chiu score. Arterial blood samples were taken for determination of plasma concentrations of TNF-α and 1L-6. Results Compared with group S, Chiu score, MDA content, MPO activity, and plasma concentrations of TNF-α and IL-6 were significantly increased, whereas SOD activity decreased in the other 4 groups ( P < 0.05). Chiu score, MDA content, MPO activity, and plasma concentrations of TNF-α and IL-6 were significantly decreased, whereas SOD activity increased in group Ipr, Ipo and Ipr + Ipo as compared with group IIR ( P < 0.05). Chiu score and MDA content were significantly lower, whereas SOD activity higher in group Ipr + Ipo than in group Ipr and Ipo ( P < 0.05). No significant differences were detected in the indices between group Ipr and group Ipo ( P > 0.05). Conclusion Ischemic preconditioning-postconditioning can attenuate the intestinal IR injury in rats, and the efficacy is better than that of either Ipr or Ipo alone.     

大鼠肠缺血再灌注损伤后肠黏膜差异表达蛋白质组的分离与鉴定

3、醛脱氢酶和醛糖还原酶,前3种酶与改善能量代谢相关,后3种酶与抗氧化应激、抑制凋亡相关.结论 建立了重复性较好的正常与II/R损伤后大鼠肠黏膜组织的双向凝胶电泳图谱.II/R的损伤机制可能与顺乌头酸酶、丙酮酸激酶、细胞色素C还原酶、蛋白二硫化物异构酶A3、醛脱氧酶和醛糖还原酶的下调有关.     

缺血预处理-后处理对大鼠肠缺血再灌注损伤的影响

Objective To evaluate the effects of ischemic preconditioning-postconditioning on the intestinal ischemia-reperfusion (IR) injury in rats. Methods Forty healthy male SD weighing 225-275 g were randomly assigned into 5 groups ( n = 8 each): group I sham operation (group S) ; group II intestinal IR (group IIR); group Ⅲ ischemic preconditioning (group Ipr); group IV ischemic postconditioning (group Ipo); group V Ipr+ Ipo. The rats were anesthetized with intraperitonel 20% urethane 5 ml/kg. Superior mesenteric artery (SMA) was occluded for 60 min followed by 60 min reperfusion. In group S, SMA was isolated but not occluded. In group Ipr, SMA was occluded for 10 min followed by 10 min reperfusion, and the rest procedures were performed using the method described in group IIR. In group Ipo, 60 min ischemia was followed by three 30 s episodes of ischemia at 30 s intervals for reperfusion. In group Ipr+ Ipo, Ipr was performed followed by Ipo and the procedures were performed using the methods described in group Ipr and Ipo. The animals were killed at 60 min of reperfusion. The intestinal tissues were immediately removed for determination of MDA content, SOD and MPO activities and the degree of damage to intestinal mucous membrane was scored according to Chiu score. Arterial blood samples were taken for determination of plasma concentrations of TNF-α and 1L-6. Results Compared with group S, Chiu score, MDA content, MPO activity, and plasma concentrations of TNF-α and IL-6 were significantly increased, whereas SOD activity decreased in the other 4 groups ( P < 0.05). Chiu score, MDA content, MPO activity, and plasma concentrations of TNF-α and IL-6 were significantly decreased, whereas SOD activity increased in group Ipr, Ipo and Ipr + Ipo as compared with group IIR ( P < 0.05). Chiu score and MDA content were significantly lower, whereas SOD activity higher in group Ipr + Ipo than in group Ipr and Ipo ( P < 0.05). No significant differences were detected in the indices between group Ipr and group Ipo ( P > 0.05). Conclusion Ischemic preconditioning-postconditioning can attenuate the intestinal IR injury in rats, and the efficacy is better than that of either Ipr or Ipo alone.     

缺血预处理-后处理对大鼠肠缺血再灌注损伤的影响

Objective To evaluate the effects of ischemic preconditioning-postconditioning on the intestinal ischemia-reperfusion (IR) injury in rats. Methods Forty healthy male SD weighing 225-275 g were randomly assigned into 5 groups ( n = 8 each): group I sham operation (group S) ; group II intestinal IR (group IIR); group Ⅲ ischemic preconditioning (group Ipr); group IV ischemic postconditioning (group Ipo); group V Ipr+ Ipo. The rats were anesthetized with intraperitonel 20% urethane 5 ml/kg. Superior mesenteric artery (SMA) was occluded for 60 min followed by 60 min reperfusion. In group S, SMA was isolated but not occluded. In group Ipr, SMA was occluded for 10 min followed by 10 min reperfusion, and the rest procedures were performed using the method described in group IIR. In group Ipo, 60 min ischemia was followed by three 30 s episodes of ischemia at 30 s intervals for reperfusion. In group Ipr+ Ipo, Ipr was performed followed by Ipo and the procedures were performed using the methods described in group Ipr and Ipo. The animals were killed at 60 min of reperfusion. The intestinal tissues were immediately removed for determination of MDA content, SOD and MPO activities and the degree of damage to intestinal mucous membrane was scored according to Chiu score. Arterial blood samples were taken for determination of plasma concentrations of TNF-α and 1L-6. Results Compared with group S, Chiu score, MDA content, MPO activity, and plasma concentrations of TNF-α and IL-6 were significantly increased, whereas SOD activity decreased in the other 4 groups ( P < 0.05). Chiu score, MDA content, MPO activity, and plasma concentrations of TNF-α and IL-6 were significantly decreased, whereas SOD activity increased in group Ipr, Ipo and Ipr + Ipo as compared with group IIR ( P < 0.05). Chiu score and MDA content were significantly lower, whereas SOD activity higher in group Ipr + Ipo than in group Ipr and Ipo ( P < 0.05). No significant differences were detected in the indices between group Ipr and group Ipo ( P > 0.05). Conclusion Ischemic preconditioning-postconditioning can attenuate the intestinal IR injury in rats, and the efficacy is better than that of either Ipr or Ipo alone.     

缺血预处理-后处理对大鼠肠缺血再灌注损伤的影响

Objective To evaluate the effects of ischemic preconditioning-postconditioning on the intestinal ischemia-reperfusion (IR) injury in rats. Methods Forty healthy male SD weighing 225-275 g were randomly assigned into 5 groups ( n = 8 each): group I sham operation (group S) ; group II intestinal IR (group IIR); group Ⅲ ischemic preconditioning (group Ipr); group IV ischemic postconditioning (group Ipo); group V Ipr+ Ipo. The rats were anesthetized with intraperitonel 20% urethane 5 ml/kg. Superior mesenteric artery (SMA) was occluded for 60 min followed by 60 min reperfusion. In group S, SMA was isolated but not occluded. In group Ipr, SMA was occluded for 10 min followed by 10 min reperfusion, and the rest procedures were performed using the method described in group IIR. In group Ipo, 60 min ischemia was followed by three 30 s episodes of ischemia at 30 s intervals for reperfusion. In group Ipr+ Ipo, Ipr was performed followed by Ipo and the procedures were performed using the methods described in group Ipr and Ipo. The animals were killed at 60 min of reperfusion. The intestinal tissues were immediately removed for determination of MDA content, SOD and MPO activities and the degree of damage to intestinal mucous membrane was scored according to Chiu score. Arterial blood samples were taken for determination of plasma concentrations of TNF-α and 1L-6. Results Compared with group S, Chiu score, MDA content, MPO activity, and plasma concentrations of TNF-α and IL-6 were significantly increased, whereas SOD activity decreased in the other 4 groups ( P < 0.05). Chiu score, MDA content, MPO activity, and plasma concentrations of TNF-α and IL-6 were significantly decreased, whereas SOD activity increased in group Ipr, Ipo and Ipr + Ipo as compared with group IIR ( P < 0.05). Chiu score and MDA content were significantly lower, whereas SOD activity higher in group Ipr + Ipo than in group Ipr and Ipo ( P < 0.05). No significant differences were detected in the indices between group Ipr and group Ipo ( P > 0.05). Conclusion Ischemic preconditioning-postconditioning can attenuate the intestinal IR injury in rats, and the efficacy is better than that of either Ipr or Ipo alone.     

麻醉药物对脑血流动力学的影响

健康成人的脑循环通过自身调节可为神经系统活动定量提供氧和葡萄糖,该自身调节会受术中麻醉用药的影响,进而改变脑的氧和能量供应.使用麻醉药物的同时控制颅内压(intracranial pressure,ICP)在正常范围,是手术安全的前提之一.颅内压由骨性颅腔的内容物,如脑组织、颅内血容量,脑脊液所决定.颅腔内容物在颅内静脉回流不受损的情况下.很大程度上取决于脑血流量(cerebral blood flow,CBF)以及脑脊液生成和吸收的平衡.麻醉药物通过多种机制改变脑血流量.     

缺血预处理抗大鼠肠缺血再灌注肠黏膜损伤的蛋白质组学研究

目的采用蛋白质组研究技术分离、鉴定缺血预处理（IPC）抗大鼠肠缺血再灌注（Ⅱ／R）肠黏膜损伤相关蛋白,探讨其肠保护分子机制。方法将16只SD大鼠,随机分为Ⅱ／R组和IPC组。Ⅱ／R组阻断肠系膜上动脉60min后再开放60min;IPC组在阻断肠系膜上动脉前先阻断20min后再开放5min。余同Ⅱ／R组。再灌注结束即刻刮取肠黏膜,利用高分辨双向电泳对肠黏膜组织进行蛋白质分离．Image Master 2D Elite 5．0图像软件进行分析。应用基质辅助电离解析飞行时间质谱获取肽质量指纹图谱．检索数据库鉴定表达差异的蛋白质,明确其生物学功能。结果双向电泳发现,Ⅱ／R组及IPC组分别有蛋白质点（1404±20）个和（1338±20）个。10个点进行质谱分析,8个蛋白质点经过检索与已知蛋白质匹配．这些蛋白功能涉及到抗氧化、抑制凋亡及改善能量代谢。RT-PCR分析提示IPC上调醛糖还原酶的表达。Western blot分析提示IPC上调醛脱氢酶的表达。结论比较蛋白组学研究揭示IPC对肠缺血再灌注损伤的保护机制可能与其上调了一些具有抗氧化、抑制细胞凋亡及改善能量代谢作用的蛋白有关。     

盐酸帕洛诺司琼预防上腹部手术后硬膜外吗啡镇痛所致的恶心呕吐

目的 观察和评价帕洛诺司琼对上腹部手术后硬膜外吗啡镇痛引起的恶心呕吐的预防效果和安全性.方法 择期行上腹部手术并术后接受硬膜外吗啡镇痛患者60例,随机分为帕洛诺司琼组（P组）和托烷司琼组（T组）.手术结束前30 min,P组患者缓慢静注帕洛诺司琼0.25 mg,T组患者缓慢静注托烷司琼6 mg.观察记录两组患者术后24 h、48 h VAS及Ramsay评分、恶心呕吐的程度,计算恶心呕吐有效控制率.同时记录患者腹胀、头痛、椎体外系症状等不良反应.结果 两组患者术后24 h及48 h的VAS及Ramsay评分差异无统计学意义.P组患者术后24 h的恶心及呕吐有效控制率分别为80.0%和73.3%,T组分别为63.3%和60.0%;P组患者术后48 h的恶心及呕吐有效控制率分别为90.0%和93.3%,T组分别为66.6%和63.3%.两组患者术后24 h恶心、呕吐有效控制率差异无统计学意义.P组患者术后48 h恶心、呕吐有效控制率明显优于T组患者（P 〈 0.05）.帕洛诺司琼的不良反应主要为头痛.结论 腹部手术后24 h内,帕洛诺司琼预防吗啡硬膜外镇痛所致的恶心呕吐的效果与托烷司琼相当,但术后48 h预防恶心呕吐的效果优于托烷司琼,且不良反应发生率低,程度较轻,安全性好.     

右旋美托咪啶对腹部手术患者全麻苏醒的影响

目的观察右旋美托咪啶分别复合七氟醚及丙泊酚对全麻患者苏醒的影响。方法选择全麻下行腹部手术患者80例,随机双盲分为4组：七氟醚＋生理盐水组（S组）、丙泊酚＋生理盐水组（P组）、七氟醚＋右旋美托咪啶组（SD组）及丙泊酚＋右旋美托咪啶组（PD组）。右旋美托咪啶用生理盐水稀释成4μg/ml,诱导插管后以3μg·kg-1·h-1静脉泵注10min,再以0.3μg·kg-1·h-1恒速维持至手术结束。S组及P组则于诱导插管后按相同速度静脉泵注生理盐水至手术结束。术中调节各组七氟醚和丙泊酚用量,以维持BIS在45±5。术后记录患者停药至睁眼的时间,并用短期定向记忆实验测量患者的认知功能。结果术后苏醒期,S组、P组和SD组的睁眼时间组间无统计学差异,但PD组患者睁眼时间较其他3组显著延长（P〈0.05）。术前及术后60min,4组患者MMSE评分差异无统计学意义。结论右旋美托咪啶不会影响患者术后的认知功能恢复,但它会延长静脉麻醉患者的苏醒时间。