Colonic Motor Activity Research Articles

Experimental Study on Gastrointestinal Motility in Inflammatory Bowel Disease.

The symptoms of urgency, diarrhea and nausea are exhibited in inflammatory bowel disease such as ulcerative colitis. The correlation among the changes of motility in gastrointestinal tracts and the symptoms were investigated using a model of acute colitis in ten dogs. Colitis was induced by acetic acid and the motility in gastrointestinal tracts was recorded with strain gauge transducers. The dogs exhibited urgency and diarrhea with mucus and blood during colitis. At the same time, the motor activity of the colon and stomach changed during colitis: 1) the incidence of colonic motor complexes (CMCs) were significantly decreased ; 2) the total duration per hour and mean duration of CMCs also decreased significantly ; 3) the incidence of giant migrating contractions (GMCs) increased significantly ; and 4) interdigestive migrating complex (IMC) of the stomach was disrupted and changed to irregular pattern. The response of colonic motility to a meal during colitis was also investigated. As the result, 1) the incidence of CMCs had a tendency to increase in the early postprandial periods in the proximal and distal colon and 2) the incidence of GMCs had similar effects to the incidence of CMCs. These findings may indicate that Gastro-Colonic Response during colitis, similarly to the normal colon, remains. There was no significant difference between the cleansed and uncleansed colon during colitis or in the normal colon. On the other hand, there was significant shortening of the mouth to caecum transit time during colitis. In conclusion, the changes in gastric and colonic motor activity, including the shortening of the mouth to caecum transit time, may be related to the abdominal symptoms accompanied by acute colitis. Moreover, the change of colonic motility including CMCs and GMCs in the early postprandial period indicates a close correlation between worseing of abdominal symptoms and up-take of meal.

Coffee and Gastrointestinal Function: Facts and Fiction: A Review

Background: Effects of coffee on the gastrointestinal system have been suggested by patients and the lay press, while doctors tend to discourage its consumption in some diseases. Methods: The literature on the effects of coffee and caffeine on the gastrointestinal system is reviewed with emphasis on gastrointestinal function. Results: Although often mentioned as a cause of dyspeptic symptoms, no association between coffee and dyspepsia is found. Heartburn is the most frequently reported symptom after coffee drinking. It is demonstrated that coffee promotes gastro-oesophageal reflux. Coffee stimulates gastrin release and gastric acid secretion, but studies on the effect on lower oesophageal sphincter pressure yield conflicting results. Coffee also prolongs the adaptive relaxation of the proximal stomach, suggesting that it might slow gastric emptying. However, other studies indicate that coffee does not affect gastric emptying or small bowel transit. Coffee induces cholecystokinin release and gallbladder contraction, which may explain why patients with symptomatic gallstones often avoid drinking coffee. Coffee increases rectosigmoid motor activity within 4 min after ingestion in some people. Its effects on the colon are found to be comparable to those of a 1000 kCal meal. Since coffee contains no calories, and its effects on the gastrointestinal tract cannot be ascribed to its volume load, acidity or osmolality, it must have pharmacological effects. Caffeine cannot solely account for these gastrointestinal effects. Conclusions: Coffee promotes gastro-oesophageal reflux, but is not associated with dyspepsia. Coffee stimulates gallbladder contraction and colonic motor activity.

Corticotropin-releasing factor and the brain-gut motor response to stress.

The characterization of corticotropin-releasing factor (CRF) and CRF receptors, and the development of specific CRF receptor antagonists selective for the receptor subtypes have paved the way to the understanding of the biochemical coding of stress-related alterations of gut motor function. Reports have consistently established that central administration of CRF acts in the brain to inhibit gastric emptying while stimulating colonic motor function through modulation of the vagal and sacral parasympathetic outflow in rodents. Endogenous CRF in the brain plays a role in mediating various forms of stressor-induced gastric stasis, including postoperative gastric ileus, and activates colonic transit and fecal excretion elicited by psychologically aversive or fearful stimuli. It is known that brain CRF is involved in the cross-talk between the immune and gastrointestinal systems because systemic or central administration of interleukin-1-beta delays gastric emptying while stimulating colonic motor activity through activation of CRF release in the brain. The paraventricular nucleus of the hypothalamus and the dorsal vagal complex are important sites of action for CRF to inhibit gastric motor function, while the paraventricular nucleus of the hypothalamus and the locus coeruleus complex are sites of action for CRF to stimulate colonic motor function. The inhibition of gastric emptying by CRF may be mediated by the interaction with the CRF2 receptors, while the anxiogenic and colonic motor responses may involve CRF1 receptors. Hypersecretion of CRF in the brain may contribute to the pathophysiology of stress-related exacerbation of irritable bowel syndrome.

The effect of electrical stimulation on colonic transit following spinal cord injury in cats.

The effect of direct electrical stimulation on colinic transit and manometric recordings following spinal cord injury were assessed in five adult male cats. Intra-colonic catheters were surgically placed, stimulating electrodes were sutured to the colonic serosa and a laminectomy with spinal cord clamping at a T4 level was done to induce spinal cord injury (SCI). Twenty radiopaque markers were inserted through an intra-colonic catheter located 1 cm distal to the cecum and were monitored with daily fluoroscopy as a measure of colonic transit. Transit measurements were compared before SCI, after SCI and after SCI with electrical stimulation of 40 pps, 1 ms, and 0-50 mA. Colonic transit following SCI was significantly prolonged (P<0.05) when compared to the transit before SCI. Electrical stimulation following SCI improved colonic transit to values not significantly different from those before SCI. Spontaneous colonic phasic motor activity was similar both before and after SCI. Manometric defection patterns were also observed to be similar before SCI and after SCI with electrical stimulation. Based on our scoring criteria, the most frequent response to electrical stimulation was an abdominal contraction. These findings demonstrate that colonic transit is prolonged following SCI and that direct electrical stimulation of the colon following SCI improves colonic transit in an animal model.

Intact colonic motor response to sudden awakening from sleep in patients with chronic idiopathic (slow-transit) constipation.

There are few data about the relationships between colonic motor behavior and higher brain functions, such as sleep. Previous studies were done in healthy subjects, and it is unknown whether patients with functional motor disorders of the colon behave differently. This study was designed to characterize colonic motor activity in patients with constipation, both during sleep and after sudden awakening, and to compare it with that of healthy subjects. Our working hypothesis was that patients with constipation would have an impaired response to sudden awakening. Twelve chronically constipated women, 22 to 49 years old, were recruited for the study, and their data were compared with those obtained from 12 healthy female volunteers, 21 to 38 years old. Manometric studies were performed in the descending and sigmoid colon for 30 minutes during sleep (immediately before awakening) and 30 minutes after being awakened suddenly. A motility index was calculated before and after the stimulus. In both groups motility in the descending and the sigmoid colon was almost absent during sleep and significantly increased after sudden awakening. No difference in postawakening values was found between patients with constipation and controls. In patients with chronic constipation, the brain-gut control of some fundamental mechanisms governing colonic motility is preserved. These data suggest that the alterations of colonic motility described in chronic constipation may be caused by an intrinsic dysfunction of the viscus.

Inhibition of stress-stimulated colonic propulsion by alpha 2-adrenoceptor antagonists in rats.

Alpha2-adrenoceptor antagonists have been reported to stimulate colonic motor activity, but the effect on colonic motor dysfunction is unclear. We have investigated the effect of alpha 2-adrenoceptor antagonists on wrap-restraint stress-stimulated and normal colonic propulsion in rats. Colonic propulsion was evaluated by the transit of a charcoal marker along the colon. Faecal pellets output was also measured. A 30-min exposure to wrap-restraint stress starting 120 min after infusion of the charcoal marker significantly stimulated colonic transit with a concomitant increase in faecal pellets. Yohimbine and idazoxan, alpha 2-adrenoceptor antagonists, clonidine, an alpha 2-adrenoceptor agonist, and atropine suppressed wrap-restraint stress-stimulated colonic transit and faecal excretion in a dose-dependent manner. Ondansetron and YM060, 5-hydroxytryptamine3 (5-HT3) receptor antagonists, potently inhibited wrap-restraint stress-stimulated colonic transit, but only weakly inhibited faecal excretion. Neither alpha 2-adrenoceptor antagonists nor atropine had any significant effect on normal colonic transit, whereas clonidine and the 5-HT3 receptor antagonists inhibited it. alpha 2-Adrenoceptor antagonists as well as clonidine, atropine and 5-HT3 receptor antagonists inhibit the stress-induced colonic motor dysfunction in rats.

Psychological and physical stress induce differential effects on human colonic motility

Objective: Stress modulates gut function, but whether the type of stressor influences colonic motor activity is unclear. The motor patterns and regional variations are also poorly understood. Our aim was to determine the effects of psychological and physical stress on colonic motility. Methods: Ambulatory colonic manometry was performed by placing a six-sensor probe up to the mid-transverse colon, without sedation, in 12 healthy subjects. Five hours later, a dichotomous listening test (psychological stress) was performed, which was preceded by listening to a narrative passage (control); recovery entailed listening to relaxing music (1 h each). Subsequently, intermittent hand immersion in cold (4°C) water (physical stress) was performed, preceded by hand immersion in warm (37°C) water ( 1 2 -h each). Colonic pressure activity and cardiovascular responses were measured throughout the study. Results: When compared with the control period, both stressors induced a greater number of pressure waves ( p < 0.05), and the area under the curve ( p < 0.01), but only physical stress increased ( p < 0.05) pulse rate and blood pressure. There were no regional differences in colonic motility. During recovery, the motor activity returned to baseline after physical stress, but remained high after psychological stress. Psychological stress induced more ( p < 0.05) propagated contractions, whereas physical stress induced more ( p < 0.05) simultaneous contractions. Conclusions: Both stressors enhanced colonic motor activity, but psychological stress induced a prolonged response with propagated activity and without appreciable autonomic response. Thus, colonic motor responses may vary depending on the stressor.

Psychological and physical stress induce differential effects on human colonic motility.

Stress modulates gut function, but whether the type of stressor influences colonic motor activity is unclear. The motor patterns and regional variations are also poorly understood. Our aim was to determine the effects of psychological and physical stress on colonic motility. Ambulatory colonic manometry was performed by placing a six-sensor probe up to the mid-transverse colon, without sedation, in 12 healthy subjects. Five hours later, a dichotomous listening test (psychological stress) was performed, which was preceded by listening to a narrative passage (control); recovery entailed listening to relaxing music (1 h each). Subsequently, intermittent hand immersion in cold (4 degrees C) water (physical stress) was performed, preceded by hand immersion in warm (37 degrees C) water (1/2-h each). Colonic pressure activity and cardiovascular responses were measured throughout the study. When compared with the control period, both stressors induced a greater number of pressure waves (p < 0.05), and the area under the curve (p < 0.01), but only physical stress increased (p < 0.05) pulse rate and blood pressure. There were no regional differences in colonic motility. During recovery, the motor activity returned to baseline after physical stress, but remained high after psychological stress. Psychological stress induced more (p < 0.05) propagated contractions, whereas physical stress induced more (p < 0.05) simultaneous contractions. Both stressors enhanced colonic motor activity, but psychological stress induced a prolonged response with propagated activity and without appreciable autonomic response. Thus, colonic motor responses may vary depending on the stressor.

Colonic Motor Activity in Women During Sleep

The relationship between colonic motility, sleep, and arousals from sleep has never been studied in women and only once in men. The purpose of this study was to determine how sleep and arousals from sleep affected colonic motility in women during the follicular phase of their menstrual cycle. We monitored sleep and segmental colonic motility in six healthy women during the follicular phase of the menstrual cycle. We observed no colonic motility during sleep; during awake periods or during arousals, we observed isolated low-amplitude bursts of colonic motility. This colonic motility occurred during 25% of the arousal and awakening time. In contrast, morning awakening was associated with high-amplitude independent and related colonic motility in all colonic segments. We conclude that in women in the follicular phase of their menstrual cycle, colonic motility is inhibited during sleep; colonic motility at night only occurs during arousals or awakenings from sleep.

Effects of acute stress on colonic motor activity and autonomic arousal in patients with constipation

Effects of acute stress on colonic motor activity and autonomic arousal in patients with constipation

Influence of mental stress and rectal distension on tonic and phasic motor activity of the left colon

Influence of mental stress and rectal distension on tonic and phasic motor activity of the left colon

Comparison of neostigmine and bethanechol effects on colonic and rectal motor activity compliance and sensation in healthy volunteers

Comparison of neostigmine and bethanechol effects on colonic and rectal motor activity compliance and sensation in healthy volunteers

Cholecystokinin (CCK) microinfused into the paraventricular nucleus of the hypothalamus (PVN) inhibits gastric emptying and stimulates colonic motor activity in the conscious rat

Cholecystokinin (CCK) microinfused into the paraventricular nucleus of the hypothalamus (PVN) inhibits gastric emptying and stimulates colonic motor activity in the conscious rat

A novel sub-classification of irritable bowel syndrome validated by differences in post-prandial colonic motor activity

A novel sub-classification of irritable bowel syndrome validated by differences in post-prandial colonic motor activity

Tonic and phasic motor activity in the proximal and distal colon of healthy humans.

In healthy humans, meals stimulate phasic and tonic motor activity in the unprepared distal colon. The response of the proximal colon remains unknown. In this study, we assessed the effect of a liquid meal on proximal and distal colonic motor activity. In 12 healthy volunteers, colonic tone and phasic motility were simultaneously recorded by using an electronic barostat and perfused catheters in the fasting state and in response to a 1,000-kcal meal. The meal significantly increased the phasic activity in the distal colon (230 +/- 46% of the basal value; P = 0.02) but not in the proximal colon (138 +/- 25% of the basal value; P = 0.2). The intrabag volume of the barostat was significantly more reduced in the distal than in the proximal colon (74 +/- 11 vs. 50 +/- 9% of the basal values, respectively; P = 0.04). We conclude that the postprandial response of the unprepared proximal colon is an immediate tonic contraction that is less pronounced than in the distal colon.

P-639 - Effect of JCM 102, a novel bisacodyl enteric seamless soft capsule, on colonic motor activity in conscious dogs

P-639 - Effect of JCM 102, a novel bisacodyl enteric seamless soft capsule, on colonic motor activity in conscious dogs

Endogenous CCK inhibits colonic contractions in unrestrained conscious rats

As cholecystokinin octapeptide (CCK-OP) and feeding have been reported to relax the circular muscle contractions of the proximal colon in unrestrained conscious rats under fasting conditions, the, action of cholecystokinin, released after duodenal infusion of a low residual diet of clinimeal, was studied on the motor activity of the proximal colon in unrestrained conscious rats. We used an implantable telemetry system with a miniature strain gauge force transducer introduced into the rat proximal colon. By using a specific radioimmunoassay system for CCK, plasma levels of CCK before and after duodenal infusion of clinimeal (0.5, 1.0, 2.0 ml) were determined at 0, 5, 10, 20, 30, 60 min in the portal blood. The clinimeal infusion caused a significant increase in CCK levels of the portal plasma during 5 and 30 min. This increase was in a dose-dependent manner. In accordance with this increase in plasma CCK, the motor activity of the proximal circular muscle was suppressed significantly. A bolus injection of the CCK A receptor antagonist, loxiglumide, CR 1505 (0.1, 0.5 and 1.0 mg/kg ip), prior to clinimeal blocked the inhibitory action of CCK on the motor activity in a concentration-dependent manner. These data suggest that endogenous CCK released by a residual diet is involved in the mechanism of inhibition of motor activity in the proximal colon.

Gastrointestinal transit and prolonged ambulatory colonic motility in health and faecal incontinence

Background—Colonic motor function has not been studied in the ambulatory setting over a prolonged period in the unprepared state. Furthermore, the disturbance of this function in patients with faecal incontinence...

Nitric oxide is involved in the inhibitory action of cholecystokinin octapeptide (CCK-OP) on proximal colonic motility

To determine whether nitric oxide (NO) is a possible mediator in the inhibitory action of CCK-octapeptide (CCK-OP) on circular muscle contractions of the rat proximal colon, contractile activities of the circular muscle were recorded in the proximal colon of unrestrained conscious rats in the fasting state using a miniature strain gauge force transducer and an implantable telemetry system. Regular and rhythmic phasic contractions were observed during the fasted condition, similar to the myoelectric migrating complex seen in intestinal contractions of the fasting dog. These phasic contractions were almost completely inhibited after intraperitoneal (i.p.) administration of CCK-OP at a dose of 15 μg/kg body weight. Nω-nitro-arginine, methyl ester ( l-NAME), at doses of 20 and 200 mg/kg i.p. administered prior to i.p. injection of CCK-OP, prevented the inhibitory action on the fasting phasic contractions. The degree of prevention was dose-dependent. 100 mg/kg body weight i.p. injection of l-arginine inhibited the circular muscle contractions. The same dose of d-arginine had no action on contractions of the circular muscle of the proximal colon in the fasted rat. From these data, we conclude that NO is one possible mediator in the inhibitory mechanism of CCK-OP on smooth muscle motor activity of the rat proximal colon in vivo.

Recurrence of Acute Colonic Pseudo-Obstruction in Selective Adrenergic Dysautonomia Associated with Infectious Toxoplasmosis

Background: Acute colonic pseudo-obstruction is a life-threatening condition associated with several pathologic conditions, whose pathophysiology is still uncertain. Case: Autonomic function in a young patient operated on for acute colonic pseudo-obstruction was carefully evaluated; none of the common clinical conditions described in the literature was found to have caused the syndrome. Selective adrenergic failure was suggested by the presence of severe orthostatic hypotension, low basal plasma catecholamine level, and absence of the expected increase on standing and by the findings of provocation tests, cardiovascular tests, and acetylcholine sweat spot test. Biopsy specimens from the colon and small-bowel wall did not show any morphologic or immunohistochemical alteration either in muscle layers or in the autonomic plexus, testifying to the possible occurrence of extrinsic denervation in the presence of an intact plexus. Infectious toxoplasmosis was proved through indirect and direct hemagglutination assays, enzyme-linked immunosorbent assay IgG, IgM, and IgA, immunosorbent agglutination IgM assay, and the protozoa were demonstrated in a biopsy specimen from the rectus abdominis muscle. Conclusions: Selective adrenergic denervation of the gut resulted in recurrent episodes of colonic pseudoobstruction, probably by direct toxicity or a cross-reaction between the immune process and a toxoplasmic antigen, stressing the importance of sympathetic inhibitory modulation on colon motor activity.