迷走神经背核对消化间期小肠肌电活动的影响

目的:研究迷走神经背核(the dorsal motor nucleus of vagus,DMV)对大鼠小肠消化间期肌电活动的影响,探讨DMV对胃肠道功能活动的调控。方法:建立大鼠DMV电刺激模型,采用双极法测定大鼠空肠的消化间期复合肌电(IMC)。分析刺激后慢波频率和振幅的变化、活动期的总持续时间及活动期与周期比值(A/T比值)的变化,刺激即时慢波与动作电位出现概率的变化。结果:电刺激DMV后大鼠空肠慢波的平均频率和平均振幅均增加(P0.05),活动期总持续时间延长(P0.01),A/T比值增大(P0.05)。刺激即时,慢波的平均频率降低、平均振幅增加(P0.01),快波出现概率增加(P0.001)。结论:电刺激致DMV兴奋,可导致大鼠小肠肌电的活动异常,这可能是DMV机能损伤引发胃肠道功能紊乱的途径之一。     

2.101 某些因素对大鼠胃肌电的影响

目的观察大鼠胃肌电的特点及某些因素对它的影响.方法将两对电极的铂丝部分沿胃的纵轴方向与环肌平行分别刺入肌层,然后将铂丝的前端约1～2mm弯曲固定在胃壁上,胃窦电极距幽门括约肌0.5cm.胃体电极距幽门括约肌1.5cm,两个电极间距为2mm.将导线通过皮下导管自两肩胛骨之间引出体外供记录用.并同时按常规方法记录体表胃电.结果 1.未禁食大鼠胃肌电特点慢波频率在4.9～5.9次/min,但振幅个体差异较大,一般5～6mV;快波,为双向不对称针形波,多以锋蔟的形式出现,振幅一般是胃窦部大于胃体部;大鼠胃肌电明显的IMC 4个时期很少,一般可根据快波的数量,振幅大小分为高活动相和低活动相.2.空腹及进食胃肌电变化禁食24h,胃体、胃窦慢波振幅略有升高,而禁食48h及禁食后进食慢波振幅较低,但无统计差异,但频率禁食后加快(P＜0 .01),快波振幅在禁食及禁食后进食均明显升高(P＜0.05～0.01),锋蔟增多,持续时间延长(P＜0.05～0.01).3.麻醉对胃肌电的影响氨基甲酸乙酯和戊巴比妥钠均使胃肌电抑制,慢波频率减少,振幅降低,快波振幅降低,锋蔟减少,持续时间缩短.两种麻醉药比较,氨基甲酸乙酯的影响比戍巴比妥钠要小,两者有统计学差异(P＜0.05). 4.体骨胃肌电与体表胃电的比较两者记录的慢波频率基本一致,但振幅差异较大,体表胃电慢波振幅为0.11～0.13mV,分别为该部位体内胃肌电的4.1%～6.5%.结论大鼠胃肌电的特点是几乎所有的慢波上都重迭有快波,根据快波数量、振幅及持续时间,一般可分为高活动相和低活动相;禁食24h快波振幅、锋蔟数及持续时间均升高,但慢波频率、振幅变化不大麻醉可使胃肌电活动减弱,氨基甲酸乙酯的抑制作用比戍巴比妥钠弱.建议麻醉用药以氨基甲酸乙酯为宜,体内胃肌电与体表胃电的慢波频率基本一致,但振幅差别很大,体内胃肌电明显高于体表胃电.     

慢性结肠无力型大鼠结肠肌电改变

目的　通过研究慢性结肠无力型大鼠结肠肌电变化 ,探讨结肠传输功能障碍的机制。方法　健康Wistar大鼠 32只 ,体重在 10 0～12 0g之间 ,雌雄各半。按照随机化原则将大鼠分为对照组、模型组 ,每组 16只。模型组通过服用复方苯乙哌啶制作慢性结肠无力型模型 ,对照组饲以普通饲料。饲养 12 0天后进行结肠肌电测定。结果　将每组的记录结果 3min作为一个时间段计算频率和振幅 ,共计 6 0个时间段。正常大鼠结肠慢波表现为不规则的近似正弦波样曲线 ,频率 13± 4 2c min ,振幅 0 19± 0 0 5 3mV。与对照组相比 ,模型组 9只大鼠结肠慢波频率明…     

长期服用苯妥英钠的癫癎患者神经电生理观察

目的:观察长期服用苯妥英钠的癫患者周围神经损害。方法:应用丹迪Neuromatic2000M型肌电仪,对37例患者进行正中神经和胫后神经的神经传导(NCV),F波和H反射的检测,同时观察肌肉的针极肌电图(EMG)。结果:癫组与对照组比较正中神经感觉速度(P<0·05),波幅(P<0·05),dML(P<0·05),F波出现率(P<0·01),胫后神经感觉波幅(P<0·05),dML(P<0·01),F波潜伏时(P<0·01)。EMG检测未发现损害。结论:长期服用苯妥英钠的癫患者可发生周围神经损害,表现为(1)感觉运动神经均有损害;(2)脱髓鞘及轴索损害都会发生,轴突损害符合远端轴突病;(3)神经损害远近端都有发生;(4)上下肢神经轴突均有损害,以下肢的轴突损害为重。     

精神分裂症患者失匹性负波(MMN)研究

目的:了解首发精神分裂症患者失匹性负波(MMN)的特征以及治疗缓解后MMN的变化。方法:应用美国Bravo脑电生理仪,记录45例首发精神分裂症患者和40名健康人的MMN,同时记录P300电位比较,并用阳性和阴性症状量表(PANSS)评定患者精神症状。患者组于治疗5周和12周时进行MMN随访。结果:(1)与正常组比较,首发精神分裂症组的MMN潜伏期延迟和波幅降低(正常组199·7±29·9ms和7·8±3·8μV,患者组221·4±32·6ms,4·5±3·3μV,P均<0·01),患者组P300中靶潜伏期P3同时延迟(P<0·01)。(2)MMN潜伏期延长和波幅低,与PANSS阳性症状和思维障碍分呈负相关(P<0·05~0·01)。(3)患者组经治疗12周后,MMN波幅呈增大改变和潜伏期缩短(P<0·01),反映患者的认知功能改善。结论:MMN技术可反映首发精神分裂症患者诱发脑电的自动加工过程。MMN可作为精神分裂症患者的临床应用检测指标。     

侧脑室注射微量五肽胃泌素对大鼠胃电和胃运动的影响

在大鼠侧脑室微量注入五肽胃泌素(G-5)0.1μg观察其对胃电和胃运动的影响。实验结果表明:侧脑室注射G-5(0.1μg/10μl)后胃电慢波的振幅由对照值的0.56mV增加到0.847mV(P<0.01),快波的振幅和频率也明显增加;胃窦运动频率增加到对照值的41.556±1.01%(P<0.01),振幅增加196.68±2.07%(P<0.001)。这一反应被切断双侧颈迷走神经所阻断。提示脑内的胃泌素可参与对胃电和胃运动的调节,这一作用可能是通过迷走神经来实现的。     

十二指肠溃疡患者上胃肠道运动及胃肠激素的研究

对30例十二指肠溃疡（Du）患者和15例正常对照者进行了消化间期移行性复合运动波（MMC）的检测及血浆胃动素（MTL）、生长抑素（SS）的放免测定．结果显示：Du患者MMC正常者仅为16．7％,明显低于对照组（60％,P＜0.001）且胃窦MMCⅢ期持续时间缩短（P＜0．05）;胃窦、十二指肠近端MMCⅡ期的收缩频率、收缩波幅均较对照组减少（P＜0.05,P＜0．001）。Du患者MMCⅡ、Ⅲ期的MTL明显低于对照组（P＜0．05）,而SS则高于对照组（P＜0．05,P＜0．55）．结果提示：胃肠道运动异常和胃肠激素的释放与Du有着密切关系。     

2.119 比较西沙必利与莫沙必利对胃和结肠运动及平滑肌细胞的收缩作用

目的已知西沙必利(cisapride)和莫沙必利(mosapride citrate)均为新一代胃肠促动力剂,两者都是苯甲酰胺衍生物,均作用于胃肠5-HT4受体促进乙酰胆碱释放 ,从而增强胃肠运动.本研究拟采用大鼠在体、离体及胃肠单个平滑肌细胞技术,比较西沙必利和莫沙必利促进胃和结肠动力作用的异同及其作用机制.方法 1.在体实验,采用清醒大鼠进行慢性实验(n=8),埋植高灵敏度应力传感器记录胃结肠消化间期移行性复合运动(MMC).应力传感器分别位于胃窦和远端结肠. 用多导生理记录仪记录、处理和分析.2.离体实验,采用大鼠离体胃窦和远端结肠的肌条( n=12)动力测定技术.用特制灌流肌槽,加进西沙必利或莫沙必利分别作用于胃窦和远端结肠的肌条,其收缩活动通过张力换能器记录在X-Y记录仪上.3.细胞实验,采用胶原酶技术分离大鼠胃窦和远端结肠的单个平滑肌细胞(n=12),观察西沙必利或莫沙必利对细胞的直接收缩作用,并比较二者作用的异同.结果 1.西沙必利与莫沙必利对胃窦和远端结肠MMC作用的比较空腹时,大鼠胃窦和远端结肠可以记录到典型的MMC活动.正常MMC Ⅲ相平均振幅为25.12±4.25g.当分别静脉给予不同剂量西沙必利或莫沙必利0.125、0 .25、0.5、1.0、2.0mg/kg时均增强胃窦和远端结肠MMC Ⅲ相收缩,两者均随剂量增加而使运动振幅逐渐增加:在胃窦,西沙必利组按上述剂量比对照组分别增加:(11.66±1. 64)%、(29.14±3.17)%、(65.68±8.95)%、(110.10±15.21)%、(142.29±18.55)% (均P＜0.01).莫沙必利组按上述相同剂量比对照组分别增加:(4.0±0.54)%、(9. 5±2.35)%、(29.89±4.67)%、(72.90±11.24)%、(81.64±14.97)%(均P＜0.0 5).在远端结肠,西沙必利组(同上述剂量)比对照组运动振幅分别增加:(38.11±3.34)% 、(62.79±7.41)%、(86.51±8.24)%、(114.41±10.34)%、(151.62±12.64)%(均 P ＜0.01).莫沙必利组(同上述剂量)比对照组分别增加:(2.31±0.81)%、(3.14±0. 60)%、(6.27±0.47)%(P＜0.05)、(8.83±1.64)%(P＜0.05)、(26.62±0. 98)%(P＜0.01).结果表明,西沙必利与莫沙必利对增加胃和结肠MMC收缩均有剂量效应关系,但西沙必利对胃窦和远端结肠的促动力作用强于莫沙必利.2.西沙必利与莫沙必利对胃窦和远端结肠平滑肌收缩活动的比较胃窦和远端结肠平滑肌正常自发收缩波振幅分别为0.32±0.07g和0.21±0.04g.西沙必利引起胃窦和远端结肠平滑肌收缩的阈浓度为0.05mg/mL,最大反应浓度为0.6mg/mL.莫沙必利的阈反应浓度为0.1mg/mL,最大反应浓度为0.6mg/mL.阈浓度时,西沙必利增加胃窦和远端结肠振幅分别为(45.16±12.25)%和(85.71±20.15)%(均P＜0.01).莫沙必利增加胃窦和远端结肠振幅分别为(25.80±6.15)%和(23.65±5.45)%(均P＜0.05).给予最大反应浓度时,西沙必利增加胃窦和远端结肠分别为(187.09±16.24)%和(328.57±46.19)% (均P＜0.01).莫沙必利增加胃窦和远端结肠分别为(125.80±21.42)%、(95.23±2 7 .36)%(均P＜0.05).结果表明,西沙必利和莫沙必利二者均可增加胃窦和远端结肠平滑肌收缩活动,但莫沙必利阈浓度比西沙比利高,莫沙必利对胃特别是远端结肠的促动力作用明显低于西沙必利.3.西沙必利与莫沙必利对胃窦和远端结肠单个平滑肌细胞作用的比较在倒置显微镜下,游离的大鼠胃窦和结肠平滑肌细胞平均长度为98μm,直径为15μm.给予促动力剂西沙必利或莫沙必利均可使平滑肌细胞长度大大缩小.西沙比利和莫沙必利引起平滑细胞收缩的阈反应浓度分别为0.125mg/mL和0.25mg/m L,最大反应浓度均为2mg/mL.二者随剂量增加而肌细胞收缩反应逐渐增加,有剂量依赖性 .在阈浓度时,西沙必利(0.125mg)引起胃肌细胞收缩(13.42±3.62)%(P＜0.01), 结肠肌细胞收缩(19.42±3.51)%(P＜0.01).莫沙必利(0.25mg)引起胃肌细胞收缩( 8.46±1.63)%(P＜0.05),结肠细胞收缩(4.86±0.96)%(P＜0.05).最大浓度时,西沙必利(2mg)增加胃肌细胞收缩(45.24±7.71)%(P＜0.01),增加结肠肌细胞收缩(51.25±6.54)%(均P＜0.01).莫沙必利(2mg)增加胃肌细胞收缩(32.14±8 .47)%(P＜0.01),增加结肠肌细胞收缩(17.43±3.52)%(P＜0.05).上述结果表明,西沙必利和莫沙必利均对胃窦和远端结肠平滑肌细胞有直接收缩作用,但前者作用比后者强.4.受体拮抗剂对西沙必利或莫沙必利增强胃窦和远端结肠收缩效应的影响给予5-HT4受体拮抗剂(GR113808(100μg/kg/mL)或胆碱能M受体阻断剂阿托品(10mg/kg/mL)均可阻断西沙必利或莫沙必利对在体、离体及细胞收缩的兴奋作用.结论西沙必利和莫沙必利均可兴奋胃窦和远端结肠运动,二者在相同剂量下,西沙必利促动力作用优于莫沙必利.西沙必利和莫沙必利均通过5-HT4受体起作用,二者对胃肠促动力强度的差异可能与其作用于胃肠的受体亚型不同有关.     

吗啡依赖及戒断对大鼠海马内神经甾体水平的影响

目的:探讨吗啡躯体依赖、精神依赖及戒断对雄性大鼠海马内神经甾体水平的影响。方法:腹腔注射递增剂量吗啡建立大鼠吗啡躯体依赖模型,纳洛酮诱发戒断症状;条件性位置偏爱实验建立吗啡精神依赖模型。高效液相色谱-质谱法测定大鼠海马和血浆中脱氢表雄酮(DHEA)及其硫酸酯(DHEAS)、孕烯醇酮(PREG)及其硫酸酯(PREGS)和别孕烯醇酮(AP)含量。结果:大鼠吗啡躯体依赖形成时海马内DHEA、PREG水平较对照组升高(0·88±0·19/0·67±0·17,t=2·52,P<0·05,10·94±2·02/7·53±2·64,t=3·24,P<0·01),血浆中DHEAS、PREGS水平较对照组升高(115·4±99·7/29·3±8·3,t=3·20,P<0·01;234·5±216·1/38·2±18·8,t=3·39,P<0·01);大鼠吗啡精神依赖形成时海马及血浆中DHEA水平降低(0·90±0·55,15·6±5·0/1·63±0·76,24·5±9·8,t=2·42,2·69,P<0·05),血浆中DHEAS水平显著升高(187·4±44·8/136·7±30·7,t=2·88,P<0·05)。与纳洛酮对照组比较,大鼠吗啡戒断时海马内DHEA、AP、DHEAS、PREGS水平升高(t=2·33~3·96,P<0·05),血浆中PREG、AP、DHEAS和PREGS水平升高(t=3·72~4·82,P<0·01)。结论:吗啡依赖、戒断可影响大鼠海马内某些神经甾体的水平,表明内源性神经甾体可能参与吗啡依赖的形成。     

自噬对大鼠肾缺血再灌注损伤的保护作用及机制

目的：观察大鼠肾脏缺血再灌注( ischemia reperfusion, I/R)损伤中肾小管上皮细胞的自噬激活情况,探讨其对肾脏I/R损伤发挥保护性作用的分子机制。方法将40只雄性Wistar大鼠随机分为4组：假手术组( Sham)、I/R组、氯喹干预组( I/R+CQ)和雷帕霉素干预组( I/R+Rap)。常规方法建立大鼠肾脏I/R损伤模型,再灌注24 h后留取各组大鼠血和肾脏标本。血标本用于尿素氮( BUN)和血肌酐( Scre)含量检测;肾组织标本行HE染色,观察病理学损伤情况;TUNEL法检测肾小管上皮细胞凋亡的改变;采用免疫组化法检测Beclin-1和Caspase-3蛋白表达,透射电镜观察大鼠肾脏自噬泡的形成情况。结果与I/R组相比,I/R+CQ组BUN和Scre明显升高(P<0．05,P<0．01),肾组织损伤积分增加(P<0．01),TUNEL阳性细胞数增多(P<0．05),Beclin-1蛋白表达减弱(P<0．01),Caspase-3蛋白表达增强(P<0．01),电镜下自噬泡数量较少(P<0．05);I/R+Rap组BUN和Scre显著降低(P<0．01),肾组织损伤积分减低(P<0．05),TUNEL阳性细胞数减少(P<0．05),Beclin-1蛋白表达增强(P<0．01),Caspase-3蛋白表达减弱(P<0．01),自噬泡数量明显增多(P<0．01)。结论自噬激活在肾脏I/R损伤过程中可通过抑制凋亡而发挥的保护作用,其机制可能涉及Beclin-1及Caspase-3等蛋白的表达调控。     

The Clinical Characteristics of Colonic Pseudo-obstruction and the Factors Associated with Medical Treatment Response: A Study Based on a Multicenter Database in Korea

Colonic pseudo-obstruction (CPO) is defined as marked colonic distension in the absence of mechanical obstruction. We aimed to investigate the clinical characteristics of CPO and the factors associated with the response to medical treatment by using a multicenter database in Korea. CPO was diagnosed as colonic dilatation without mechanical obstruction by using radiologic and/or endoscopic examinations. Acute CPO occurring in the postoperative period in surgical patients or as a response to an acute illness was excluded. CPO cases were identified in 15 tertiary referral hospitals between 2000 and 2011. The patients'' data were retrospectively reviewed and analyzed. In total, 104 patients (53 men; mean age at diagnosis, 47 yr) were identified. Seventy-seven of 104 patients (74%) showed a transition zone on abdominal computed tomography. Sixty of 104 patients (58%) showed poor responses to medical treatment and underwent surgery at the mean follow-up of 7.4 months (0.5-61 months). Younger age at the time of diagnosis, abdominal distension as a chief complaint, and greater cecal diameter were independently associated with the poor responses to medical treatment. These may be risk factors for a poor response to medical treatment.

Graphical Abstract

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结肠癌的蛋白质组学研究

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