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Gastrointestinal motility is a major field of research. However, despite a huge amount of data available in the literature, its exact role has yet to be defined. This paper deals with the choice of animal research models for motility studies.
Any determination of gastrointestinal motility is based on two assumptions: (1) That the patient is examined in "physiological" conditions and (2) that the values measured truly reflect the parameter the investigator wishes to examine. A large array of very different drugs shares the ability to modify the digestive motility (i.e. gastrokinetics) or to alter the content of the digestive tube in such a way that it affects the outcome of some measurements (i.e. acid suppression leads to false results in ph-metry dependent methods). Therefore, it seems advisable to ask the patient whether he is taking any drug--including non prescription medications--and check if this substance or type of substances could affect the outcome of the motility measurement envisioned. In this paper, the authors present a list of the principal drugs known to affect different motility-measurement methods. The real or apparent stimulating or inhibitory effects of drugs on four main segments of the digestive tube (esophagus, stomach, small intestines and colon) are indicated in an alphabetically ordered table. In a short review, the drugs are broadly classified according to their mechanism and site of action. Besides a number of drugs used in practice because of their action on the enteric nervous system, there is a large spectrum of compounds affecting motility, whose main therapeutic application lies outside the digestive tract, such as: psychotropic drugs, antiparkinsonian drugs, bronchodilators, antitussives, antihistamines, antimigraine drugs, antihypertensive agents, etc. This second category is more likely to escape unnoticed as a potential source of false results in the measurement of digestive motility.
Gastrointestinal motility of young broilers (1, 8 and 15 days old) was measured by means of 14C-polyethylene glycol-4000. Two motor patterns can be observed: GI segments anterior to ileum increased their motility proportionally to the broiler age. GI segments below ileum decreased their motility when the broiler age is increased. It is concluded that these motor patterns are due to immaturity of gastric motility, early learning of food intake regulation and/or interference between prenatal and postnatal nutrition. Proventriculus and duodenal loop showed to be transit segments, with independence of the broiler age.
The interest of gastroenterologists in the relationship between Helicobacter pylori and gastrointestinal motility emerges from the observation that Helicobacter pylori may be involved in the pathogenesis of functional dyspepsia and that a relatively large percentage of patients with dyspepsia may show impaired gastrointestinal motility. A number of studies have been published on the interaction between Helicobacter pylori infection and gastrointestinal motility with controversial results, and, therefore, there are no definite conclusions, as yet, as to whether Helicobacter pylori is able, at all, or in which degree, to influence the motility of the upper gastrointestinal tract. Motility of the upper gastrointestinal tract has been studied in Helicobacter pylori positive and negative individuals by means of manometry, scintigraphy, radio-opaque markers or by other, recently developed, procedures such as breath tests, ultrasonography, and barostat. The vast majority of studies do not support the hypothesis that Helicobacter pylori may influence gastrointestinal motility. Nearly all these studies are, however, affected by methodological problems related to the small numbers of patients, different methodological approaches, and to the well-known difficulties in studying both gastrointestinal motility and functional dyspepsia.
Caring for children with gastrointestinal motility disorders requires an understanding of age-related changes in gastrointestinal function and in the clinical expression of disease. Successful evaluation of the child with a gastrointestinal motility disorder necessitates an approach that takes into account not only the child's symptoms, but also the stage of development. This article reviews the ontogeny of gastrointestinal motility; the techniques available for the study of gastrointestinal motility in children; and the presentation, pathophysiology, and treatment of pediatric functional bowel diseases. Differences in children compared to adults in performing and analyzing motility testing and in evaluating motility disorders are emphasized. A more complete understanding of pediatric motility disorders may provide important insights in approaching functional bowel diseases in adults.
A radiological study has been carried out in the dog to control the influence of N-ethyl-2(2-methoxy-5-sulfamido-benzamidomethyl)-pyrrolidine (sulpiride) on the motility of the gastrointestinal tract. The drug was administered orally and parenterally at different doses for each pharmaceutical form and for such route of doses for each pharmaceutical form and for each route of administration. In doses which were considered optimal, the results have demonstrated that sulpiride exerts hypertonic and hyperphasic effects on the smooth musculature of the gastrointestinal tract. Consequently, there is a reduction of the transit time and of the emptying of the opaque meal in the various sectors of the gastrointestinal tract, which is in the order of about 50% with respect to normal. Using doses which are inferior to those considered optimal, no significant results were obtained, while following higher doses the action of sulpiride is manifested by an inhibitory effect on gastrointestinal motility.
Gastrointestinal motility and plasma PYY levels were investigated under chronic progressive large bowel obstruction in dogs. The obstruction device was applied around the descending colon at a laparotomy and gastrointestinal motility was recorded with strain gauge force transducers in the conscious state. Complete obstruction occurred at 26 days (21-33 days). The duration of postprandial interruption of motor complex (DIMC) in the antrum and duodenum were prolonged progressively, at partial obstruction (17.7 +/- 2.7 hr; p less than 0.05) and complete obstruction (23.0 +/- 4.0 hr; p less than 0.01) vs in control (13.7 +/- 1.9 hr), while DIMC in the small bowel showed no significant changes. Progressive obstruction caused hypermotility in the proximal colon to the obstruction and hypomotility in the distal colon. These dysmotility were improved after resection of the obstructed segment and anastomosis. Plasma PYY levels in the fasting state showed no significant increase at complete obstruction (42.6 +/- 14.5 pmol/l) vs in control (32.9 +/- 10.2 pmol/l).
AIM: To isolate the proteins involved in pharmacologic action of senna extract (SE) from mouse gastrointestinal tract and to explore the molecular mechanism of gastrointestinal motility change induced by SE. METHODS: SE was administrated to mice by different routes. Gastrointestinal motility of mice was observed using cathartic, gastrointestinal propellant movement experiments and X-ray analysis. Mouse model for gastrointestinal motility enhancement was established through continuous gastric administration of SE at progressively increased dose. At 3 h and week 3, 4, 6 and 10, morphological changes of gastrointestinal tissues were found under light microscope. Ultrastructural changes of intestinal and colonic tissues at week 6 were observed under transmission electron microscope. The colonic proteomic changes in model mice were examined by two-dimension polyacrylamide gel electrophoresis with immobilized pH gradient isoelectric focusing to screen the differentially expressed proteins, and their molecular masses and isoelectric points were determined. Two N-terminal sequences of the samples were also determined by mass spectrometry. RESULTS: SE (0.3g) caused diarrhea after gastric administration in 1-6h and enhanced gastrointestinal propellant (65.1+/-7.5%; 45.8+/-14.6%, P<0.01) in mice, but intramuscular and hypodermic injection had no cathartic effect. X-ray analysis of gastrointestinal motility demonstrated that gastric administration of SE enhanced gastric evacuation and gastrointestinal transferring function. At 3 h and week 3 and 4 after gastric administration of SE, light microscopic examination revealed no apparent change in gastrointestinal mucosal tissues, but transmission electron microscopic examination revealed inflammatory changes in whole layer of intestinal and colonic wall. Twenty differential proteins were detected in the colonic tissues of the model mice by two-dimensional electrophoresis, and the N-terminal amino acid sequences of two proteins were determined. CONCLUSION: SE causes diarrhea and enhances gastrointestinal motility through digestive tract administration. Long-term gastric administration of SE induces inflammatory changes and cell damage in the whole gastrointestinal tract. The differential proteins screened from the colonic tissues of the model mice might mediate the enhancing effect of SE on gastrointestinal motility.
Ileus is common during sepsis; however, the etiology of this gastrointestinal dysmotility is unclear. The aim of our study was to determine the effects of a single, sublethal dose of endotoxin on canine gastrointestinal motility, gastric emptying, gastric acid secretion, and colonic transit. Six dogs underwent placement of manometric catheters in the stomach and small bowel and insertion of a gastric and a cecal cannula. After the animals recovered, fasting and fed gastrointestinal motility was recorded, and gastric emptying and colonic transit were studied with nonabsorbable liquid and solid markers, respectively. Following completion of baseline studies, each dog was given a single dose of Escherichia coli lipopolysaccharide (200 micrograms/kg intravenously) and the studies were repeated on Postendotoxin Days 1-3. The single bolus of endotoxin abolished the migrating motor complexes, decreased the fasting motility index, decreased hydrogen ion output, slowed liquid gastric emptying, and prolonged colonic transit for 2 days. Gastrointestinal motility and transit returned to baseline on Postendotoxin Day 3. In conclusion, a single, sublethal dose of endotoxin temporarily disrupts fasting and postprandial canine gastrointestinal motility and transit.
PURPOSE: To review the pathophysiology of gastrointestinal motility disorders during pregnancy, their clinical manifestations, and their management. DATA SOURCES: Studies published from 1963 to 1992 identified by computerized literature searches of Index Medicus and MEDLINE; hand searches; contact with pharmaceutical representatives for information on drug therapy during pregnancy; and selected texts on drugs and obstetrics. STUDY SELECTION: Selected studies were those involving controlled design of physiology related to pregnancy or to hormonal effects on the gastrointestinal tract or both, and clinical studies or previous reviews that contributed to the understanding of the gastrointestinal effects of pregnancy. DATA EXTRACTION: Data concerning the epidemiology, causes, clinical manifestations, and complications of altered gastrointestinal motility during pregnancy as well as the strength of association between gastrointestinal disorders of pregnancy and hormonal changes were evaluated and used to develop a practical approach to evaluate and manage these patients. RESULTS OF DATA SYNTHESIS: Effects on the gastrointestinal tract during pregnancy are caused primarily by hormonal changes and not the physical effects of the gravid uterus. Motility changes occur throughout the gastrointestinal tract, including a reduction in lower esophageal sphincter pressure and its physiologic function with resulting gastroesophageal reflux and the risk for aspiration; alterations in gastric motor function associated with nausea and vomiting; and a decrease in the rate of small-bowel and colonic transit manifested primarily as abdominal bloating and constipation. These effects are mediated by progesterone, with estrogen probably acting as a primer. CONCLUSIONS: Given the large number of pregnancies each year complicated by gastrointestinal motility disorders, many physicians (including internists and gastroenterologists) must manage these problems. Knowledge of the underlying physiologic alterations in gastrointestinal motility during pregnancy and of safe treatment options is essential to the care of the pregnant patient.
Gastrointestinal symptoms such as vomiting, constipation, diarrhea, and fecal incontinence occur frequently in patients with diabetes mellitus. In a survey of 136 diabetic outpatients, 76% had one or more gastrointestinal symptoms, the commonest symptom being constipation (found in 60%). In many cases these symptoms are thought to be due to abnormal gastrointestinal motility that, in turn, may be a manifestation of diabetic autonomic neuropathy involving the gastrointestinal tract. The pathophysiology of these gastrointestinal symptoms, clarified in recent studies, and the clinical features and treatment of these problems in diabetic patients are reviewed.
A classification of gastrointestinal motility disorders is offered based upon the type of disorder in transit (delay or acceleration), and the region of the gastrointestinal tract affected. Specific abnormalities of myoelectrical patterns are identified when possible and related to disturbances in transit in the stomach and small bowel.
OBJECTIVE: To investigate the pathogenesis of gastrointestinal motility dysfunction as a result of scald and lipopolysaccharide (LPS) challenge in guinea pigs. METHODS: Thirty guinea pigs were enrolled in the study and were randomly divided into 3 groups:i. e. control (n = 10, with intraperitoneal injection of isotonic saline), scald (n = 10, with 30% TBSA deep partial thickness burn) and LPS (n = 10, with intraperitoneal injection of LPS) groups. Thirty minutes after treatment, all animals were gavaged with carbolic ink. The propelled distance of the ink within the gastrointestinal tract was measured. The intestinal tissue was harvested and homogenized, and the contents of CGRP, Na+-K+-ATP enzyme, Mg2+-ATP enzyme, Ca2+-ATP enzyme, Ca2+-Mg2+-ATP enzyme were determined, and the delta phim of haustra coli smooth muscular cell mitochondria was assessed. RESULTS: The propelled distance of the ink in the gastrointestinal tract in scald (53 +/- 9 cm) and LPS (91 +/- 10 cm) groups was obviously shorter than that in control group (142 +/- 11 cm, P < 0.01). Furthermore, the distance in scald group was shorter than that in LPS group (P < 0.01). The CGRP content in scald and LPS groups [52.0 +/- 39.0 microg/L and 20.0 +/- 23.0 microg/L] was obviously higher than that in control group (0.8 +/-2.0 microg/L, P <0.05 or 0.01), especially in scald group ( P < 0.05). The Na+-K+-ATP enzyme, Mg2+-ATP enzyme, Ca2+-ATP enzyme, Ca2+-Mg2+-ATP enzyme and the delta phim in scald and LPS groups were remarkably lower than those in control group (P <0.005), but there was no difference between scald and LPS groups (P > 0.05). CONCLUSION: The gastrointestinal motility of guinea pigs could obviously be inhibited by scald and LPS, especially by scald. LPS might be the key factor to produce change in the membrane potential of mitochondria of intestinal smooth muscle after severe scald.
The effects of loperamide on gastrointestinal motility were investigated in conscious fasted dogs chronically fitted with strain-gauge transducers on the antrum, the jejunum, and the colon. Oral administration of loperamide (0.1 mg/kg) induced, after a delay of 20-30 min, a long-lasting (8-12 hr) stimulation of gastrointestinal motility associated with a disorganization of the cyclic activity at the three levels investigated. These effects were reproduced by a subcutaneous administration at the same dose and were antagonized by previous intravenous administration of naloxone or a quaternary opiate antagonist. Intracolonic administration (0.1 mg/kg) stimulated, after a delay of 20-30 min, colonic motility only. Intracerebroventricular loperamide (1 microgram/kg) induced a long-lasting (15-20 hr) inhibition of the gastric motility and a short (2-hr) disorganization of the jejunal motor profile. These data show that oral loperamide stimulates gastrointestinal motility in dogs and involves peripheral opiate receptors.
The use of laparoscopic surgery contributes to faster recovery of postoperative gastrointestinal motility. Several authors have demonstrated the benefits of laparoscopic surgery using carbon dioxide (CO2) pneumoperitoneum. However, there have been few investigations of the effects of other insufflation gases on gastrointestinal motility. The aim of this study was to investigate the effect of CO2 and helium pneumoperitoneum on the recovery of postoperative gastrointestinal motility. For this study, male Sprague-Dawley rats were divided into four groups: control, CO2 insufflation (10 mmHg), helium insufflation (10 mmHg) and open laparotomy for one hour. Arterial pH values and PaCO2 were measured after surgery. Gastrointestinal motility was evaluated by quantifying the distribution of markers placed into the stomach at the end of procedures until 24 hours after surgery. In the CO2 insufflation group, the arterial pH value was significantly lower than that of the helium insufflation group, and significant hypercapnia persisted until six hours after surgery. The gastric emptying and transit time was significantly prolonged in the CO2 group compared with the helium insufflation group. This study demonstrates that helium pneumoperitoneum can improve the recovery of postoperative gastrointestinal motility because of the reduction of hypercapnia and a tendency to suffer acidosis compared with CO2 pneumoperitoneum.
A technique of combined hepatobiliary scintigraphy and gastrointestinal motility recordings was used to study the relationship between gallbladder dynamics and gastrointestinal motility recordings in the postprandial state in eight healthy male volunteers. In all, a fed-like motility pattern was observed after ingestion of a standard meal, and all activity from the HIDA-scintigraphy was diverted to the duodenum. Gallbladder radioactivity on the scintigram was not seen until 145-249 (median, 180) min after ingestion, except for two cases in which an early and transient activity was seen. Together with increasing gallbladder radioactivity characteristic changes in duodenal motility occurred. In five subjects a decrease in motility index was encountered with a motility curve resembling phase I of the interdigestive migrating motor complex. In one subject it was associated with the appearance of a phase-III complex, and in two subjects it occurred without any changes in motility index.
The control mechanisms of gastrointestinal motility are complex. Extrinsic neurohormonal effects modulate an intrinsic system, often called the "gut brain," composed of nervous and neuropeptide components. To exert pharmacologic influence on GI motility, use is made of agents that mimic the external control system. Agents that stimulate opioid receptors, block adrenoceptors, block or facilitate acetylcholine action, or antagonize the action of prostaglandins are used to effect changes in GI motility. The major indications for pharmacologic intervention are to increase motility in constipation, to reduce it in most cases of diarrhea, and to restore propulsive coordination in postoperative ileus. In cases of clinical colic the primary requirement is control of pain. Agents used for this purpose may adversely affect motility, and choice requires knowledge of their actions in this respect. In addition, drugs used for other purposes, anthelmintics for instance, may also influence gut motility. A synopsis of the actions of the agents commonly employed in GI motility control and some associated drugs are displayed in Table 3. Recent advances in the understanding of drug action on the gut should help in the selection of drugs for clinical use.
The mechanism of gastric stasis in disorders of gastrointestinal motility is largely unexplored. The region or regions of abnormal motility in 13 patients with a gastrointestinal motility disorder were characterized manometrically. Antral hypomotility was established in 6 patients and intestinal dysmotility in 7 others. One patient had both antral hypomotility and intestinal dysmotility. Gastric emptying of solids and liquids was quantitated scintigraphically; emptying data for solids were represented by a two-phase model (lag and emptying) and for liquids by a power exponential model. Antral hypomotility was associated with gastric stasis manifested by both a prolongation of the solid lag time [from 35 +/- 6 min for controls to 87 +/- 23 min (mean +/- SE), p less than 0.05] and slower emptying rates of solids (from a slope index of 29.9 +/- 2 for controls to 17.8 +/- 5, p less than 0.05) and liquids (from a kappa index of 3.6 +/- 0.6 for controls to 1.5 +/- 0.5, p less than 0.05). Intestinal dysmotility did not alter the solid lag time; however, it did decrease the slope of solid emptying from the stomach (from a slope index of 29.9 +/- 2 for controls to 13.5 +/- 3, p less than 0.05) and also prolonged emptying of liquids (from a kappa index of 3.6 +/- 0.3 for controls to 1.9 +/- 0.6, p less than 0.05). These data are consistent with the hypothesis that the gastric stasis in gut dysmotilities occurs because of impaired antral peristalsis due to antral hypomotility or increased resistance to flow into the small bowel due to intestinal dysmotility.