Colonic motility diagnosis based on colonic pressure

Manometry of the alimentary tract is a valuable and widely used means to evaluate and diagnose the function of the alimentary tract. However, the measurement can be inconvenient due to the invasive method used, and the many factors affecting results. Research on colonic pressure data is even more insufficient. This paper deals with colonic pressure data via an improved method ensuring that pressure data of the whole colon is available. The data is analysed based on the learning vector quantization (LVQ) method. Testing results show that this method distinguishes the normal data and the abnormal data, consistently with the original diagnoses. This method can serve as an assistant diagnosis of colonic motility and contributes to further research on colonic motility based on pressure data.     

Colonic pressure data processing based on independent component analysis

The Colonic manometry is an important technique to evaluate human colonic motor functions, which are critical for doctors to understand the pathology of intestinal diseases like slow transit constipation (STC) and colonic inertia (CI). However, in the obtained pressure signals, several patterns of colonic motor activities as well as noises mixed together, which made it difficult to observe the information people really needed. In this article, a new method was proposed to extract patterns of colonic motility from the mixed signals, so that researchers could study them thoroughly. Colonic pressure recordings from 26 volunteers were obtained by the water-perfused manometry catheters. Then independent component analysis (ICA) was introduced, which successfully separated colonic motility patterns and noises into four independent components. And according to the rhythm of contractions examined by ICA, subjects' colonic motility could be divided into three types: regular rhythm (12 subjects), slow rhythm (8 subjects) and disordered (6 subjects), which exactly accorded with their original diagnosis.     

人体结肠压力信号的HHT分析

结肠测压技术可以提供结肠动力活动的信息.是广泛使用的评价消化道功能的检查手段.但是人体结肠压力信号具有明显的非平稳性,并且测量时难以避免外界的高频干扰,传统的时域观察或者频域分析很难对测压结果进行准确的分析.本文采用希尔伯特-黄变换(HHT)对临床采集的28例结肠压力信呼进行分析.先将人体结肠压力信号通过经验模式分解(EMD)方法分解为一系列自适应的固有模式函数(IMF),然后判断并提取出其中主要的分量c3,对其进行Hilbert变换,得出时间-频率-幅值(能量)表示的三维Hilbert时频谱及其边际谱,真实准确地反映出结肠压力信号蕴含的特征信息.依据来自于医学上现有的结肠动力理论进行分析判断,结果表明,这种分析方法对于区分出正常(5例)和异常(23例)人体结肠压力信号有明显的作用.结果符合现有理论,说明HHT是一种分析结肠压力信号的有效方法.     

Central orexin-A increases colonic motility in conscious rats

Increasing evidence has indicated that brain orexin plays a vital role in the regulation of gastrointestinal physiology such as gastric secretion, gastric motility and pancreatic secretion. However, little is known whether orexin in the brain is involved in the physiology of the lower gastrointestinal tract. The aim of this study was therefore to elucidate whether orexin-A in the brain is involved in the regulation of colonic motility. In this study, we measured fecal pellet output and recorded intraluminal colonic pressure waves in freely moving conscious rats to evaluate the effects of central orexin-A on colonic motor functions. Intracisternal but not intraperitoneal injection of orexin-A dose-dependently (1-10 μg) increased fecal pellet output. Findings obtained from manometric recordings revealed that intracisternal administration of orexin-A at a dose of 10 μg significantly enhanced colonic motor contractions. These results suggest for the first time that orexin-A acts centrally in the brain to enhance fecal pellet output and stimulate colonic motility in conscious rats. The present study would furthermore support our hypothesis that orexin-A in the brain may be an important candidate as a mediator of the cephalic phase gut stimulation including stimulated colonic motility in addition to well known physiological response such as stimulation of gastric acid and pancreatic acid secretion, and gastric motility.     

Effects of neurotensin, substance P and methionine-enkephalin on colonic motility

The influence of neurotensin, substance P and methionine-enkephalin (met-enkephaline) on proximal and distal colonic motility was studied in anesthetized cats. When administered i.v, at a dose of 14 pmol x kg-1 x min-1, neurotensin increased basal smooth muscle tone and antiperistaltic activity in the proximal colon. After higher doses of neurotensin the basal muscle tone also increased in the distal colon. Substance P at a dose of 17 pmol x kg-1 x min-1 selectively and powerfully stimulated the distal colon, thus causing a mass contraction pattern with a concomitant decrease in peristaltic amplitude. In the proximal part of the colon 17 pmol x kg -1 x min-1 of substance P exerted an inhibitory action on the peristaltic amplitude in animals with a high level of spontaneous activity. In addition, the basal muscle tone was slightly decreased. In animals with sluggish spontaneous activity, however, no effects were detected in the proximal colon. With increasing doses of substance P forceful contractions of the proximal colon were also registered. Met-enkephalin at a dose of 40 pmol x kg-1 x min-1 increased the smooth muscle basal tone with no effect on the peristaltic activity in the proximal or distal segments. The effect on basal tone was blocked by naloxone. Thus, neurotensin, substance P and met-enkephalin have distinct motor actions on the colon. At low doses neurotensin may stimulate the churning and mixing functions of the proximal colon. Substance P exerts its major effects on the distal part with a mass contraction response and met-enkepahlin increases the basal muscle tone equally in the proximal and distal parts of the colon.     

Psychoneurogastroenterology: interrelations in stress-induced colonic motility and behavior

Individual differences in behavioral and physiological response patterns to stress may contribute to vulnerability for stress-related illnesses such as functional gastrointestinal disorders. Animal models could give clues about specific individual determinants of intestinal reactivity to stress and stress-induced sensitization. Rats fitted with permanent electrodes on the proximal colon were exposed to a single session of foot shocks (10 x 6 s in 15 min, preshocked) or no shocks (control). Two weeks later, the preshocked group showed a significantly greater colonic spike burst response to a novel shock-prod stressor in the home cage than controls. The increase in burst frequency was positively correlated with the duration of active burying of the threatening prod in both experimental groups, but not with other behavioral components. Basal colonic burst frequency at rest was negatively correlated with the increase in burst frequency due to shock-prod stress in both groups, but the degree of sensitization in preshocked rats vs. controls was of similar magnitude in rats with low and high basal colonic burst frequency. The results indicate that colonic responsivity to stress is related to both basal motility status and individual coping strategies.     

Colonic patch and colonic SILT development are independent and differentially regulated events

Intestinal lymphoid tissues have to simultaneously ensure protection against pathogens and tolerance toward commensals. Despite such vital functions, their development in the colon is poorly understood. Here, we show that the two distinct lymphoid tissues of the colon—colonic patches and colonic solitary intestinal lymphoid tissues (SILTs)—can easily be distinguished based on anatomical location, developmental timeframe, and cellular organization. Furthermore, whereas colonic patch development depended on CXCL13-mediated lymphoid tissue inducer (LTi) cell clustering followed by LTα-mediated consolidation, early LTi clustering at SILT anlagen did not require CXCL13, CCR6, or CXCR3. Subsequent dendritic cell recruitment to and gp38⁺VCAM-1⁺ lymphoid stromal cell differentiation within SILTs required LTα; B-cell recruitment and follicular dendritic cell differentiation depended on MyD88-mediated signaling, but not the microflora. In conclusion, our data demonstrate that different mechanisms, mediated mainly by programmed stimuli, induce the formation of distinct colonic lymphoid tissues, therefore suggesting that these tissues may have different functions.     

Influences on colonic and small intestinal motility by the cerebellar fastigial nucleus.

The fastigial influence on intestinal motility was investigated in acute experiments on chloralosed cats. Motility was recorded both from the small and large intestine. Electrical stimulation of the rostral fastigial pole produced, in combination with a blood pressure rise, increased motor activity in ileum and colon while jejunum could respond with either increased on decreased motility. The intestinal responses were neither secondary to changes in intestinal blood flow, nor to baroreceptor reflexes induced by the increased blood pressure. The excitatory responses were not due to increased parasympathetic activity since sectioning of such pathways failed to abolish the responses. Instead, interruption of adrenergic sympathetic discharge, accomplished either by guanethidine or by sectioning of relevant nerves, aid eliminate the responses, indicating that the fastigial effects were mediated by suppression of prevailing adrenergic tone. Noxious stimuli to the abdomen, including laparotomy, inhibit intestinal motility by a reflex increase in adrenergic discharge. It is suggested that fastigial influence on intestinal motility is mainly due to suppression of this reflex.     

Effect of substance P on colonic mechanoreceptors, motility, and sympathetic neurons

Intracellular recording techniques were used in vitro to analyze the effects of substance P (SP) on synaptic transmission and electrical properties of sympathetic neurons in the inferior mesenteric ganglion (IMG) of the guinea pig. Intraluminal pressure-recording techniques were used to study the effects of SP on colonic motility. Superfusion of the ganglia with SP (10(-7) to 10(-6) M) depolarized the cell soma (2--12 mV) and increased cell input resistance (8--11 M omega). These effects converted synchronous excitatory postsynaptic potentials, in response to electrical stimulation of preganglionic nerves, and asynchronous excitatory postsynaptic potentials, in response to activation of colonic mechanoreceptors, to action potentials. Administration of SP to only the colon increased basal intraluminal pressure and the frequency and amplitude of phasic changes in intraluminal pressure. These changes increased mechanoreceptor synaptic input to neurons in the IMG. We conclude that SP facilitates synaptic transmission along noradrenergic pathways and increases colonic motility.     

Chronic restraint stress has no more stimulatory effects on colonic motility in rats

Previous studies have shown that acute stress stimulates colonic motor function via a central corticotropin releasing factor (CRF) in rodents. However, little is known whether colonic motility is altered following chronic stress. We studied the changes of colonic motor function in response to chronic stress or daily administration of CRF in rats. Rats were subjected to restraint stress for 90 min for 5 consecutive days (chronic stress). Another group of rats received intracisternal (IC)-injection of CRF (1 μg) for 5 consecutive days. At the 1st day of restraint stress, calculated motility index was significantly increased by over 200% of basal in the proximal and distal colon. Similar results were obtained in response to the 2nd and 3rd day of restraint stress. In contrast, at the 5th day, restraint stress caused no more significant increase of colonic motility. Similarly, accelerated colonic transit induced by acute stress was no more observed following chronic stress. Increased, colonic motility and accelerated colonic transit induced by CRF were not attenuated at the 5th day. It is suggested that adaptation mechanism is developed following chronic stress. The decrease in colonic motor function in chronic stress is not due to reduced sensitivity to central CRF.     

Colonic epithelial cell proliferation in a rat model of nongenotoxin-induced colonic neoplasia.

BACKGROUND: The effect on colonic cell proliferation of poligeenan, a nongenotoxic polysaccharide that induces colon tumors in rats, was compared with guar gum and carrageenan. EXPERIMENTAL DESIGN: Fischer 344 rats were fed a basal diet supplemented with carrageenan and poligeenan fibers for up to 91 days. The quantitative levels of proliferation, location of the proliferating cells, and the ability of the mucosa to readapt by removing the experimental fibers from the diet were tested. RESULTS: The mucosal epithelium exhibited a 5-fold increase in thymidine kinase activity in both the carrageenan and poligeenan groups. Proliferating cells appeared at the luminal surface only in the poligeenan-treated rats, and the number of proliferating cells in the upper third of the crypt increased 35-fold. A second and third set of animals were fed one of the three test diets for either 28 or 64 days, followed by a 28-day recovery period. Proliferation in the guar- and carrageenan-treated groups returned to basal levels. In poligeenan-treated rats, thymidine kinase levels, and proliferating cells in the upper third of the crypt remained 2- and 11-fold, respectively, above controls. CONCLUSIONS: The difference in recovery time between the poligeenan group and the others, and the luminal location of proliferating cells may prove useful as markers in understanding early events in the carcinogenic process induced by a nongenotoxin.     

An experimental study of the diurnal changes in colonic motility centering on defecation]

The following findings have been obtained as a result of making an assessment regarding the diurnal changes in colonic motility by means of continuous measurement of contractile waves by using strain gauge force transducers and roentgenographic observation in conscious dogs. 1. Before defecation, the contractile force of the wave was weak, frequency of its emergence was also small, and transfer of intestinal content was slow, showing decrease of colonic motility. 2. After defecation, the gradually increasing and decreasing contractile wave groups became clear, and the contractile force was intensified concurrently with increase of its emerging frequency. Transfer of intestinal content to the anal side was rapid, and recovery of colonic motility was observed. 3. The recovery of the colonic motility after defecation was observed regardless of digestive or interdigestive state. 4. By intake of food, increase of the colonic motility corresponding to gastrocolic response was observed, but it was due to the increase of emerging frequency of contractile wave, for which no change was observed in contractile force or duration in each individual waves. 5. It was suggested that the contractile motion which undergoes gradual increase and decrease is the basic pattern in the colonic motility and that the colonic motility changes by the differences of amount, shape and hardness of intestinal content, and decreases gradually along with increase of intestinal content, but the basic pattern of contractile motion is restored by inflow of intestinal content into the colon which became empty after defecation. From the above it was considered to be inadequate to use the pattern classification of digestive and interdigestive state for the analysis of colonic motility and that assessments should be made centering on defecation.     

一种基于结肠压力的结肠动力性能诊断方法的研究

消化道测压是其他检查手段不可替代的，广泛使用的评价消化道运动功能的检查手段，对消化道运动障碍型疾病的诊断有较高的价值。但由于测量压力均是介人性检查，实施起来很不方便，且影响因素较多，所以对结果的分析还需要不断积累经验。结肠压力测量的研究更是如此。本研究对实际采集的结肠压力信号进行特征提取，采用学习矢量量化的方法进行结肠压力信号的识别。学习结果表明，这种方法可以将结肠压力信号分为正常和异常两组，与初始的医疗诊断相符合，为进一步根据结肠压力信号识别肠道的动力性能奠定了基础。     

Effect of itopride hydrochloride on the ileal and colonic motility in guinea pig in vitro

PURPOSE: Itopride hydrochloride (itopride) inhibits acetylcholinesterase (AChE) and antagonizes dopamine D(2) receptor, and has been used as a gastroprokinetic agent. However, its prokinetic effect on the small bowel or colon has not yet been thoroughly investigated. The aim of this study was to investigate the effects of itopride on motor functions of the ileum and colon in guinea pigs. MATERIALS AND METHODS: The distal ileum was excised and the activity of peristaltic contraction was determined by measuring the amplitude and propagation velocity of peristaltic contraction. The distal colon was removed and connected to the chamber containing Krebs-Henseleit solution (K-H solution). Artificial fecal matter was inserted into the oral side of the lumen, and moved toward the anal side by intraluminal perfusion via peristaltic pump. Colonic transit times were measured by the time required for the artificial feces to move a total length of 10 cm with 2-cm intervals. RESULTS: In the ileum, itopride accelerated peristaltic velocity at higher dosage (10(-10)-10(-6) M) whereas neostigmine accelerated it only with a lower dosage (10(-10)-10(-9) M). Dopamine (10(-8) M) decelerated the velocity that was recovered by itopride infusion. Itopride and neostigmine significantly shortened colonic transit at a higher dosage (10(-10)-10(-6) M). Dopamine (10(-8) M) delayed colonic transit time that was also recovered after infusion of itopride. CONCLUSION: Itopride has prokinetic effects on both the ileum and colon, which are regulated through inhibitory effects on AChE and antagonistic effects on dopamine D(2) receptor.     

Immunohistological differential diagnosis of inflammatory colonic diseases

Immunohistological investigations were carried out on human colonic tissue from, I healthy mucosa, 2 slightly inflamed mucosa, 3 mucosa with ulcerative colitis, 4 mucosa with Crohn's colitis, using antibodies against immunoglobulins and complement components. All our antibodies, including F(ab')2 fragments, demonstrated a progressive increase of labelled cells from healthy mucosa through slightly inflamed mucosa to mucosa with ulcerative colitis, in contrast to a complete absence of labelled cells in cases of Crohn's disease. The results are discussed with regard to their pathogenesis and their clinical significance for the differentiation of ulcerative colitis and Crohn's colitis.     

ATP介导的嘌呤能信号在阿尔茨海默病相关结肠运动障碍中的作用

目的:探讨ATP介导的嘌呤能信号在阿尔茨海默病(Alzheimer’s disease,AD)相关结肠运动障碍中的作用及其相关的分子机制。方法:(1)临床试验:收集我院20例AD患者进行研究,放射免疫法测定血浆中胃动素(motilin,MTL)、胆囊收缩素(cholecystokinin,CCK)、血管活性肠肽(vasoactive intestinal peptide,VIP)和一氧化氮(nitric oxide,NO)水平;高效液相色谱法(high-performance liquid chromatography,HPLC)检测血浆三磷酸腺苷(adenosine triphosphate,ATP)水平,同时对患者进行神经心理学检查并积分。(2)动物实验:利用AD小鼠进行Morris水迷宫实验,评估空间学习记忆功能;放射免疫法测定血浆中MTL、CCK、VIP和NO水平,HPLC法检测血浆ATP水平;免疫组织化学法检测乙酰胆碱转移酶(choline acetyltransferase,ChAT)、VIP、一氧化氮合酶(nitric oxide synthase,NOS)和ATP合酶的变化;Western blot和免疫组化法检测P2Y受体表达水平的变化。(3)离体实验:离体器官浴槽系统观察P2Y受体激动剂α,β-亚甲基ATP(α,β-methylene ATP,α,β-MeATP)对自发性及电刺激诱导的结肠平滑肌收缩的影响,细胞内微电极技术观察α,β-MeATP对结肠平滑肌细胞膜电位的影响。结果:与对照组比较,AD患者血浆的MTL和CCK水平明显降低(P0.01),NO和ATP水平显著升高(P0.05或P0.01),VIP无明显变化。患者简明精神状态检查积分(MMSE)降低(P0.05),AD评定量表-认知分量表(ADAS-Cog)积分、神经精神问卷(NPI)积分和AD协作研究日常能力量表(ADCS-ADL)积分均明显高于对照组(P0.01)。AD小鼠4~6 d逃逸潜伏期明显延长(P0.05),空间探索能力明显降低(P0.05),AD小鼠血浆中MTL和CCK水平明显降低(P0.01),NO和ATP水平显著升高(P0.05或P0.01),VIP无明显变化,AD小鼠结肠表达ATP合酶的水平明显上调(P0.05),但ChAT、VIP和NOS无明显改变,同时P2Y受体表达水平升高(P0.01)。体外实验表明,α,β-MeATP呈浓度依赖性抑制对照组和AD组小鼠结肠平滑肌自发性收缩(P0.05或P0.01),且这种抑制作用可被Na+通道阻断剂河豚毒素(tetrodotoxin,TTX)逆转(P0.05或P0.01),α,β-MeATP在100μmol/L时对AD小鼠自发性收缩的抑制作用更明显(P0.05),AD小鼠与正常小鼠比较,TTX对100μmol/L的α,β-MeATP的拮抗作用差异也有统计学显著性(P0.05)。在10 Hz电刺激诱导的结肠平滑肌收缩中,α,β-MeATP抑制正常小鼠和AD组小鼠的收缩(P0.05或P0.01),且40μmol/L和100μmol/L时对AD小鼠的抑制作用比正常小鼠明显(P0.05或P0.01)。平滑肌细胞膜电位实验显示,α,β-MeATP不影响结肠平滑肌膜电位(P0.05)。结论:AD患者和AD小鼠血浆中促进胃肠运动的激素MTL和CCK水平降低,抑制胃肠运动的激素NO水平升高,胃肠总体运动功能被抑制;AD小鼠血浆ATP水平升高,同时ATP嘌呤能神经元增加,P2Y受体表达上调;在AD发病中,ATP介导的嘌呤能信号可能通过抑制结肠平滑肌收缩,从而导致结肠运动功能障碍。     

Mechanisms involved in colonic vasoconstriction and inhibition of motility induced by neuropeptide Y

Neuropeptide Y (NPY) and noradrenaline are suggested to coexist as neurotransmitters in sympathetic neurons. The present study investigated the mechanisms involved in the colonic vasoconstriction and inhibition of motility induced by infusion of NPY and noradrenaline close i.a. Colonic blood flow was monitored using a drop recorder, and motility was registered by a volume recording device, both operating an ordinate writer. Colonic motility was stimulated either by electrical stimulation of the pelvic nerves (PNS; 4 Hz, 5 ms, 8 V) acting via enteric ganglia or by i.v. infusion of bethanechol (10 nmol kg-1 min-1) acting directly on muscarinic receptors on smooth muscle. With both types of motility stimulation, an immediate colonic vasodilatation was registered. Electrical stimulation of the lumbar colonic nerves (4 Hz, 5 ms, 8 V) induced colonic smooth muscle relaxation and vasoconstriction during continuous PNS (P less than 0.05). Colonic contraction induced by PNS (P less than 0.01) was dose-dependently reduced by NPY (50-400 pmol min-1; P less than 0.05-0.01) and noradrenaline (1000-6000 pmol min-1; P less than 0.05-0.01). Simultaneously, vasoconstriction was induced by both NPY and noradrenaline (P less than 0.01). Colonic contraction induced by infusion of bethanechol (P less than 0.01) was not inhibited by NPY (50-200 pmol min-1). However, at the highest dose (400 pmol min-1) the motility response was reduced (P less than 0.05). Similarly, noradrenaline only at the highest dose (6000 pmol min-1) reduced the contractile response (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)