胃泌素、胃动素测定在胃肠疾病中的意义

<正> 胃泌素和胃动素测定临床已经应用于消化疾病的诊断,但迄今为止,这两种激素在胃肠的一些疾病,特别是胃、十二指肠粘膜病变的疾病中,到底起何作用仍不为临床所认同,各家报道亦不一致。我们测定了部分胃、十二指肠粘膜病变患者及正常人血中胃泌素(GAS)和胃动素(MTL)水平,以探讨GAS和MTL在胃肠疾病中的临床意义。     

鸡屎藤水提液促胃肠动力作用的实验研究

目的探讨鸡屎藤水提液促进胃肠运动功能的影响。方法采用在体肠推进性运动和胃排空实验方法以及离体肠管和胃实验方法,研究鸡屎藤水提液对肠、胃运动功能的影响。结果鸡屎藤水提液高、中、低剂量(10.0、5.0、2.5 g生药/kg)组对胃内残留率均明显降低,与蒸馏水组相比差异显著(P 0.05),对小肠推进百分比也明显提高,与蒸馏水组相比差异也显著(P 0.05);离体实验中,鸡屎藤水提液给药后的肠管平滑肌收缩的振幅显著高于给药前,与给药前相比差异显著(P 0.01),胃底环形肌的收缩频率和幅度显著高于给药前,与给药前相比差异显著(P 0.01)。结论鸡屎藤水提液具有促进肠推进性运动和胃排空的作用。     

兔胃电活动的观察

目前,胃肠电活动的研究十分活跃。胃肠道激素的研究进展很快;但是,这些物质对胃肠电活动的影响研究者较少。这是今后消化道运动生理的重要课题。为此,我们用在胃窦部埋植电极的方法,观察记录兔的胃电活动和异博定等药物对胃电活动的影响,为探讨胃肠电活动的规律提供资料。     

慢性间歇运动对功能性消化不良的康复影响

研究慢性间歇运动对功能性消化不良的康复影响,选择某医院住院的90名功能性消化不良患者作为研究对象,随机将其划分成慢性间歇运动组和对照组,令两组进行相应的实验方案。结果:慢性间歇运动组实验后胃泌素(GAS)、胃动素(MTL)、分泌型免疫球蛋白A(Sig A)和白细胞介素2(IL-2)均明显高于实验前和对照组,差异具有显著统计学意义。实验后慢性间歇运动组血浆胰高糖素(GLU)和血管活性肠肽(VIP)明显低于实验前与对照组,差异具有显著统计学意义。结论是慢性间歇运动有助于功能性消化不良的康复。     

眶额叶区多巴胺对胃运动的影响及其机制研究

通过大鼠眶额叶微量注射给药,记录胃内压(Intragastric pressure,IGP),观察胃运动变化的方法,研究了眶额叶多巴胺(dopamine,DA)对胃运动调节的神经机制.结果显示,眶额叶注射DA10μg,胃内压显著升高;眶额叶单独注射DA D1受体阻断剂SCH 2μg(SCH23390,SCH),胃内压降低.眶额叶注射SCH 2μg,能阻断DA升高胃内压的作用;眶额叶注射利陪酮(Risperidon)2μg,可升高胃内压,增强胃运动.但利陪酮却不能阻断DA升高胃内压的作用;切断双侧膈下迷走神经,眶额叶注射DA增加胃内压的作用被消除.以上各组中胃收缩频率均无明显变化.实验结果表明,眶额叶内DA能增大胃内压,增强胃运动,DA对胃内压及胃运动的增强作用主要是通过D1受体介导,经过迷走神经传出.     

小波变换模极大值重建方法消除胃电检测中的运动伪迹

在体表测得的胃电信号受到被试身体移动的影响会产生运动伪迹;这些高幅值的运动伪迹给胃电信号的提取带来了不稳定性。该文引入小波变换模极大值重建方法去除信号中的运动伪迹。采用多孔算法对信号进行小波变换,根据筛选准则去除运动伪迹对应的小波变换模极大值点,再根据标架理论,采用共轭梯度算法由模极大值重建信号,就达到了去除运动伪迹的目的。实验表明,此方法可以有效去除胃电信号中的运动伪迹。结果也说明在胃电信号的提取中,该方法可以作为一种有效的预处理方法,促进胃电在研究和临床中的应用。     

小波变换模极大值重建方法消除胃电检测中的运动伪迹

在体表测得的胃电信号受到被试身体移动的影响会产生运动伪迹;这些高幅值的运动伪迹给胃电信号的提取带来了不稳定性。该文引入小波变换模极大值重建方法去除信号中的运动伪迹。采用多孔算法对信号进行小波变换,根据筛选准则去除运动伪迹对应的小波变换模极大值点,再根据标架理论,采用共轭梯度算法由模极大值重建信号,就达到了去除运动伪迹的目的。实验表明,此方法可以有效去除胃电信号中的运动伪迹。结果也说明在胃电信号的提取中,该方法可以作为一种有效的预处理方法,促进胃电在研究和临床中的应用。     

民族常用药娘孜泽苦寒伤胃作用研究——对胃肠运动功能的影响

目的:研究民族常用药娘孜泽苦寒伤胃,对胃肠运动功能的影响,以期指导药物临床安全用药.方法:配制营养性半固糊,观察不同娘孜泽组分部位(水提物、生物碱部位及非生物碱部位)对正常小鼠胃排空和小肠推进功能的影响.结果:(1)动物出现蜷缩、嗜睡、精神状态差、自发活动减少等症状,水提部位和生物碱部位有少量动物死亡,解剖发现胃肠胀气明显;(2)娘孜泽水提物和生物碱部位能明显增加胃部营养糊的残留量,减少营养糊在小肠的推进距离,缩短小肠推进率,胃肠运动功能抑制明显,尤以生物碱部位0.180g/kg抑制作用最强.结论:娘孜泽具有明显的胃肠苦寒毒性,尤以其生物碱部位苦寒作用最为明显.     

民族常用药娘孜泽苦寒伤胃作用研究——对胃肠运动功能的影响

目的: 研究民族常用药娘孜泽苦寒伤胃, 对胃肠运动功能的影响, 以期指导药物临床安全用药. 方法: 配制营养性半固糊, 观察不同娘孜泽组分部位(水提物、生物碱部位及非生物碱部位)对正常小鼠胃排空和小肠推进功能的影响. 结果: (1)动物出现蜷缩、嗜睡、精神状态差、自发活动减少等症状, 水提部位和生物碱部位有少量动物死亡, 解剖发现胃肠胀气明显; (2)娘孜泽水提物和生物碱部位能明显增加胃部营养糊的残留量, 减少营养糊在小肠的推进距离, 缩短小肠推进率, 胃肠运动功能抑制明显, 尤以生物碱部位0.180g/kg抑制作用最强. 结论: 娘孜泽具有明显的胃肠苦寒毒性, 尤以其生物碱部位苦寒作用最为明显.     

三种麻醉剂对大鼠离体胃肠平滑肌收缩性影响的比较研究

把大鼠离体小肠段和离体胃的浸浴液(台氏液)分别换成含不同麻醉剂的台氏液．用二道记录仪记录平滑肌的收缩曲线．以收缩频率、平均幅度、运动指数和抑制率为指标,判断三种麻醉剂对离体胃肠平滑肌收缩性的影响,并进行比较．结果表明,三种麻醉剂对大鼠离体胃肠平滑肌收缩性都有不同程度的抑制作用．氨基甲酸乙酯对离体胃平滑肌收缩性的抑制作用最大,抑制率为95．6％;水合氯醛的抑制作用最小,抑制率为56．4％;然而,水合氯醛对离体十二指肠平滑肌收缩性的抑制作用最大,抑制率为99．5％;戊巴比妥钠的抑制作用最小,抑制率为48．9％．建议如进行麻醉大鼠胃运动的中枢调控机制的研究,宜采用水合氯醛麻醉;如进行麻醉大鼠小肠运动的中枢调控机制的研究,宜采用戊巴比妥钠麻醉．     

Induction and organization of Ca2+ waves by enteric neural reflexes.

The motility of the gastrointestinal tract consists of local, non-propulsive mixing (pendular or segmental) and propulsive (peristaltic) movements. It is generally considered that mixing movements are produced by intrinsic pacemakers which generate rhythmic contractions, and peristalsis by intrinsic excitatory and inhibitory neural reflex pathways, but the relationship between mixing and peristalsis is poorly understood. Peristalsis is compromised in mice lacking interstitial cells of Cajal, suggesting that these pacemaker cells may also be involved in neural reflexes. Here we show that mixing movements within longitudinal muscle result from spontaneously generated waves of elevated internal calcium concentration which originate from discrete locations (pacing sites), spread with anisotropic conduction velocities in al directions, and terminate by colliding with each other or with adjacent neurally suppressed regions. Excitatory neural reflexes control the spread of excitability by inducing new pacing sites and enhancing the overall frequency of pacing, whereas inhibitory reflexes suppress the ability of calcium waves to propagate. We provide evidence that the enteric nervous system organizes mixing movements to generate peristalsis, linking the neural regulation of pacemakers to both types of gut motility.     

Effect of electroacupuncture in Weijing points on gastrointestinal interdigestive migrating motor complex and brain gut peptides release in dogs

Interdigestive gastrointestinal migrating motor complex (MMC) activities were recorded by strain gauge implanted on the serosa in 7 conscious dogs. We studied the effects of electroacupuncture (EAP) Weijing points Zusanli (S36), Tianshu (S25), Liangmen (S21) on MMC and release of motilin and gastrin, and compared them with that of EAP Pangguangjing points. The results indicated that EAP Weijing points could not only strengthen MMC contractions in antrum, duodenum and proximal jejunum, but also increase plasma concentration of motilin and gastrin. Anti-motilin serum, proglumide, atropine, or hexamethonium could markedly block the effect of EAP on reinforcing MMC contraction and release of motilin and gastrin. We could get the conclusions that such enhancing effect of EAP Weijing points on MMC and brain-gut peptides release is mediated by motilin and gastrin, on which both cholinergic nerve and sympathetic nerve play important roles.     

Evidence that substance P is a neurotransmitter in the myenteric plexus

Substance P (SP) is an undecapeptide originally isolated from the gut and since shown to occur within neurones in several parts of the peripheral and central nervous systems. Immunohistochemical studies indicate an exceedingly dense network of SP-containing nerves within the myenteric plexus of the guinea pig ileum. These nerves are intrinsic to the gut wall and can release SP to contract the longitudinal muscle layer. We have previously shown that SP directly depolarizes myenteric neurones and that this depolarization has a time course and ionic mechanism similar to the slow excitatory postsynaptic potential (e.p.s.p.) which can be produced by electrical stimulation of presynaptic nerves within the myenteric ganglia. We wondered whether SP might mediate this slow synaptic potential. We report here that the SP depolarization and the slow e.p.s.p. are reversibly depressed by chymotrypsin, an enzyme which degrades SP, although the responses to acetylcholine, serotonin and an unknown hyperpolarizing transmitter are unaffected. The results provide direct evidence that a peptide can mediate chemical transmission between neurones in the mammalian nervous system.     

低聚果糖和低聚异麦芽糖促进斑马鱼肠道蠕动作用的研究

探讨基于斑马鱼模型的低聚果糖及低聚异麦芽糖对肠道蠕动的促进作用。选用发育正常的5 d的斑马鱼幼鱼,各实验组分别加入不同浓度的低聚果糖和低聚异麦芽糖溶液,培养24 h后,在显微镜下观察其对斑马鱼肠道蠕动次数的影响。实验结果表明,125~500 mg/mL的低聚果糖和低聚异麦芽糖均对斑马鱼肠道蠕动有促进作用,蠕动次数与浓度成正相关性。相同浓度条件下,低聚果糖较低聚异麦芽糖促进斑马鱼肠道蠕动的作用更明显。采用斑马鱼动物模型可实现促进肠蠕动药物的早期、快速筛选。     

Role of cyclic AMP in a serotonin-evoked slow inward current in snail neurones

One model of synaptic transmission suggests that transmitters modify postsynaptic permeability through the intermediary of cyclic AMP. Thus, serotonin (5-hydroxytryptamine) evokes in molluscan neurones a decrease in a voltage-dependent K+ conductance which in turn generates a slow inward current when studied in steady voltage-clamp conditions. The serotonin-induced increase of the plateau phase of the spike of an Aplysia sensory neurone can be mimicked by both intracellularly injected cyclic AMP and extracellularly applied phosphodiesterase inhibitors, suggesting that cyclic AMP mediates the effect. We have tested whether a similar mechanism could account for the serotonin slow inward current in identified snail neurones and have found that the intracellular injection of cyclic AMP, but not of cyclic GMP or 5'-AMP, evokes a slow inward current showing similar voltage dependence, inversion potential and ionic properties to the serotonin slow inward current. Phosphodiesterase inhibitors at low concentrations (1-20 microM) potentiate the serotonin slow inward current and at higher concentrations evoke by themselves an inward current, partially or totally occluding the serotonin and cyclic AMP currents. Finally, we have found that in homogenates of pooled identified snail neurones serotonin stimulates the adenylate cyclase, increasing its activity by 50-100%.     

基于小波分析的结肠蠕动压力信号提取方法

为了获取纯净的结肠蠕动信号,提出了一种基于小波分析的结肠蠕动压力信号提取方法.其中,对结肠压力信号进行5层的小波分解,去除干扰信号后重构信号,进而获得结肠蠕动压力信号.同时,针对异常的结肠压力数据进行了验证实验.结果表明:所提出的方法对异常的结肠压力信号具有很好的抑制效果,并可以保留结肠蠕动压力信号的细节特征;与含突变信号的结肠蠕动压力信号相比,所提取的结肠蠕动压力信号的信噪比较高、均方误差较低.     

Universal physical responses to stretch in the living cell

With every beat of the heart, inflation of the lung or peristalsis of the gut, cell types of diverse function are subjected to substantial stretch. Stretch is a potent stimulus for growth, differentiation, migration, remodelling and gene expression. Here, we report that in response to transient stretch the cytoskeleton fluidizes in such a way as to define a universal response class. This finding implicates mechanisms mediated not only by specific signalling intermediates, as is usually assumed, but also by non-specific actions of a slowly evolving network of physical forces. These results support the idea that the cell interior is at once a crowded chemical space and a fragile soft material in which the effects of biochemistry, molecular crowding and physical forces are complex and inseparable, yet conspire nonetheless to yield remarkably simple phenomenological laws. These laws seem to be both universal and primitive, and thus comprise a striking intersection between the worlds of cell biology and soft matter physics.     

大熊猫胃肠道内分泌细胞的形态学研究

为了解大熊猫胃肠道内分泌细胞的形态特点，本文用ＰＡＰ法对两只大熊猫胃底、幽门腺区、十二指肠、空肠、回肠、结肠和直肠的五羟色胺、生长抑素、胃素、胆囊收缩素、神经降压素、胃动素、抑胃多肽、胰高血糖素、血管活性肠肽和内啡肽免疫反应阳性细胞进行了研究。     

胃炎消冲剂对水杨酸致大鼠萎缩性胃炎的治疗作用

目的用大鼠实验性慢性萎缩性胃炎动物模型,观察中药复方胃炎消冲剂对此模型的治疗作用.方法用改良的水杨酸灌胃法制备慢性萎缩性胃炎模型.以三九胃泰为阳性对照药,观察胃炎消冲剂对模型大鼠胃酸分泌,胃蛋白酶活性,胃肠蠕动功能及胃粘膜病理变化的影响.结果胃炎消冲剂可明显提高慢性萎缩性胃炎模型大鼠的胃液酸度,增强胃蛋白酶活性,减轻胃粘膜萎缩,对胃肠排空速度无影响.结论胃炎消冲剂可提高胃液酸度及胃蛋白酶粘性对大鼠实验性慢性萎缩性胃炎有显著的治疗作用,且不影响胃肠蠕动功能.其疗效优于三九胃泰.     

An antidepressant that extends lifespan in adult Caenorhabditis elegans

The mechanisms that determine the lifespan of an organism are still largely a mystery. One goal of ageing research is to find drugs that would increase lifespan and vitality when given to an adult animal. To this end, we tested 88,000 chemicals for the ability to extend the lifespan of adult Caenorhabditis elegans nematodes. Here we report that a drug used as an antidepressant in humans increases C. elegans lifespan. In humans, this drug blocks neural signalling by the neurotransmitter serotonin. In C. elegans, the effect of the drug on lifespan is reduced or eradicated by mutations that affect serotonin synthesis, serotonin re-uptake at synapses, or either of two G-protein-coupled receptors: one that recognizes serotonin and the other that detects another neurotransmitter, octopamine. In vitro studies show that the drug acts as an antagonist at both receptors. Testing of the drug on dietary-restricted animals or animals with mutations that affect lifespan indicates that its effect on lifespan involves mechanisms associated with lifespan extension by dietary restriction. These studies indicate that lifespan can be extended by blocking certain types of neurotransmission implicated in food sensing in the adult animal, possibly leading to a state of perceived, although not real, starvation.