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PubMedDate not supplied

Gastrointestinal motility testing--a personal perspective.

The role of motility tests in the evaluation of some common disorders in which motility has been assumed to play a role is reviewed. Three separate areas, non-cardiac chest pain, constipation and the irritable bowel syndrome are discussed. In each area, considerable difficulty in the clinical definition of these disorders persists and presents a major obstacle to the evaluation of diagnostic tests. With regard to non-cardiac chest pain, it is apparent that gastro-oesophageal reflux and sensory/perception abnormalities, rather than dysmotility, are the predominant factors, and investigations should take account of this. While studies of colonic and small intestinal motility have demonstrated various abnormal patterns in patients described as suffering from the irritable bowel syndrome, the specificity of any of these motor 'abnormalities' remains uncertain, and manometry cannot be recommended as a diagnostic tool in this context. Considerable advances have been made in our understanding of gut motor physiology and in our ability to accurately record motor function in man, the basic pathophysiology of many 'functional' gut syndromes remains unclear, and the role of dysmotility, in particular, poorly defined.

Chest Pain↗
PubMed1985

Neurotensin: a central neuromodulator of gastrointestinal motility in the dog.

The effects of intracerebroventricular and intravenous injection of neurotensin on gastrointestinal and colonic motility were examined in fasted and fed conscious, intact, and vagotomized dogs. When administered intracerebroventricularly at 20 ng X kg-1 or higher doses in the fasted state, neurotensin reduced the duration of the periods of gastric motility for 3-4 h. During this time the jejunal migrating motor complex was replaced by isolated phases of regular activity occurring at a rhythm of 2-3/h, while colonic motility was unaffected. These effects were abolished after vagotomy and were not observed for 25 times higher doses when administered intravenously. Injected intracerebroventricularly at a dose of 100 ng X kg-1 30 min after a meal, neurotensin significantly reduced (P less than 0.01) the duration of the fed pattern (2.7 +/- 0.7 vs. 8.7 +/- 1.2 h for control); this effect was not observed when neurotensin was administered intracerebroventricularly 20 min before or 120 min after a meal or when injected intravenously. Systemic administration of neurotensin at a dose of 500 ng X kg-1 significantly increased (P less than 0.05) during 2 h the colonic motility indexes in both fasted and fed dogs before and after vagotomy. It is concluded that neurotensin can act i) centrally to control the pattern of antral and jejunal motility in the fasted and fed dogs, these effects being mediated by the vagus; and ii) peripherally to control the pattern of colonic motility, this response being unaffected by vagotomy.

Animals↗
PubMed1987

[Effect of circadian rhythm on gastrointestinal motility].

In western civilization, circadian rhythms of the gastrointestinal tract are dominated by a digestive-interdigestive rhythm: During the day interdigestive activity is rare because of frequent meal intakes prior to termination of preceding fed states: in contrast, nocturnal activity is largely interdigestive. Digestive and interdigestive functions are characterized by specific and interactive motor and secretory activity patterns. When exogenous influences via food intake are prevented, additional, underlying, endogenous, circadian rhythms are observed that modulate gastric and intestinal motility in a characteristic fashion, possibly with tight links to the central nervous system. It is likely that disturbances of physiologic circadian modulation of gastrointestinal function may have pathogenic importance.

Animals↗
PubMed1992

Effect of midecamycin acetate on gastrointestinal motility in humans.

The effect was studied on gastrointestinal motor activity of three different macrolides (erythromycin, roxithromycin and midecamycin acetate), administered by mouth in therapeutic doses. This placebo-controlled study was performed in 12 normal human subjects by means of intraluminal pressure measurements in the gastric antrum, duodenum and upper jejunum. In each subject, three manometries were done for 5 h in the interdigestive period and for 3 h postprandially. In the interdigestive period, midecamycin acetate did not affect the characteristics of the gastric migrating motor complex (MMC) and did not increase the number of antral contractions or the gastric motility index as compared to the placebo. Erythromycin and roxithromycin increased the number of antral contractions (24.5 +/- 11 versus 15.2 +/- 7 and 28.4 +/- 12 versus 14.9 +/- 5.9 respectively) and the motility index (4.05 +/- 0.5 versus 3.17 +/- 0.6 and 4.38 +/- 0.2. versus 3.64 +/- 0.7 respectively) as compared to the placebo. In the postprandial period, the number of antral contractions was not significantly increased by any of the three antibiotics. The postprandial antral motility index was not significantly increased by midecamycin acetate. In contrast, the postprandial antral motility indexes after erythromycin (4.4 +/- 0.5) and after roxithromycin (4.3 +/- 0.2) were significantly greater than after the placebo. In the upper small intestine, erythromycin elicited an increased number of phase-III-like activity events and roxithromycin shortened the MMC cycle length. Midecamycin acetate had no effect on interdigestive upper jejunal motility. The postprandial jejunal motor activity was not altered by any of the three antibiotics neither during the interdigestive nor the postprandial periods.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

Fetal gastrointestinal motility in a rabbit model of gastroschisis.

PURPOSE: Gastrointestinal (GI) dysmotility occurs frequently in full-term infants with gastroschisis (GS). Although controversial, preterm delivery of infants with GS has been advocated to prevent the development of GI dysmotility, and understanding the etiology of gestational-related bowel injury may lead to prenatal therapies. Using a fetal rabbit model, the authors assessed in vivo and in vitro GI motility in preterm GS fetuses. METHODS: On gestation day 24 (term, 31), surgery was performed in maternal rabbits and GS induced in fetuses, whereas control fetuses underwent sham procedures. On gestation day 29, both groups of fetuses received ultrasound-guided intragastric injection of fluorescein and colored microspheres. Two hours after injection, fetuses were delivered by cesarean section and stomach and small intestine harvested intact. "GI motility" was calculated as the distance traveled by fluorescein divided by total length. In vitro studies of fetal gastric muscle strips contractility responses to bethanechol, a cholinergic agonist, were assessed in an organ bath system. Data were analyzed as paired and unpaired t tests and expressed as means +/- SEM. RESULTS: GS reduced fetal body weight and intestinal length compared with controls (28.4 +/- 1.4 v. 33.5 +/- 1.5 g, 36.9 +/- 1.8 v. 25.9 +/- 1.2 cm; P <.05, respectively). Fetuses with GS showed markedly reduced in vivo GI motility (51.4 +/- 2.9 v 24.8 +/- 2.7%; P <.05) and in vitro gastric contractile tension (769 +/- 53 v 396 +/- 26 mNcm2; P <.05). CONCLUSIONS: GI exposure to amniotic fluid reduces intestinal motility and gastric contractility functions in the preterm rabbit fetus. The results suggest that GS-associated impairment of GI neuromuscular functions occurs in utero, before term, and may be responsive to manipulation of amniotic fluid content or other therapeutic interventions.

Amniotic Fluid↗
PubMed1981

Guts and their motions (gastrointestinal motility in health and disease).

In the last decade, a much greater understanding of human upper intestinal motility has been obtained. The existence of a cyclical fasting pattern is now recognized, associated with intermittent secretion and propulsion of material through the stomach and small intestine. This pattern changes after the ingestion of food, the duration of the disruption depending upon both quality and quantity of nutrient ingested. The present clinical relevance of this phenomenon is twofold. 1) In normal fasting persons, the passage and absorption by the small intestine of food and drugs may be influenced by such periodic changes. 2) Motility abnormalities in disease states may account for associated gastrointestinal symptoms. While the number of disorders showing clinically relevant motor dysfunction is small, continuing study will undoubtedly bring others to light, and may even provide a rational basis for therapy.

Bacterial Infections↗
PubMed2004

The use of botulinum toxin for the treatment of gastrointestinal motility disorders.

Botulinum toxin type A is used extensively for the management of gastrointestinal smooth muscle disorders. This review is a comprehensive summary of the current status of this therapy. It includes English-language research from 1966 to 2003 and relevant abstracts from subspecialty meetings from the past 3 years. Botulinum toxin appears to be beneficial for achalasia, gastroparesis, sphincter of Oddi dysfunction, anal fissure and anismus. Very few placebo-controlled trials have been performed despite widespread use of toxin for the past 10 years. Botulinum toxin appears to be safe and side effects are uncommon. Despite uncontrolled data, botulinum toxin is now used for a variety of spastic disorders of GI smooth muscle. In some instances this therapy may preclude the need for more invasive treatments. Controlled trials are needed.

Anti-Dyskinesia Agents↗