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PubMed1990

Dopamine interrupts gastrointestinal fed motility pattern in humans. Effect on motilin and somatostatin blood levels.

The aim of this study was to investigate the hypothesis that during the postprandial period in humans, dopamine interrupts the gastrointestinal motility pattern through a mechanism that is peptide-mediated. Fourteen normal human subjects were studied by means of intestinal manometry. After recording two consecutive migrating motor complexes a 900-kcal solid-liquid meal was given. In eight subjects 30 min after the meal, placebo or dopamine (5 micrograms/kg/min) was infused for 15 min and then the recording continued for 120 min. In the remaining six subjects dopamine was administered twice with a 90-min interval in between. In three subjects the first dopamine infusion after the meal was preceded by treatment with placebo, the second by domperidone (20 mg intravenous as bolus), in the other three subjects domperidone was given before the first dopamine infusion. Blood samples for the determination of somatostatin and motilin were drawn basally, during, and immediately after dopamine in seven subjects. The results show that dopamine interrupts the fed motility pattern, inhibiting the high antral waves, and activates a duodenal phase III of migrating motor complexes. The pretreatment with domperidone completely prevented the dopamine effect. Plasma levels of motilin increased significantly during dopamine, while somatostatin blood levels did not change. These findings support the hypothesis that a dopaminergic mechanism may modulate the cycling of duodenal motor complex in humans.

Adult↗
PubMed2006

Novel smooth muscle markers reveal abnormalities of the intestinal musculature in severe colorectal motility disorders.

Histopathological studies of gastrointestinal motility disorders have mainly focused on enteric nerves and interstitial cells of Cajal, but rarely considered the enteric musculature. Here we used both classical and novel smooth muscle markers and transmission electron microscopy (TEM) to investigate muscular alterations in severe colorectal motility disorders. Full-thickness specimens from Hirschsprung's disease, idiopathic megacolon, slow-transit constipation and controls were stained with haematoxylin/eosin (HE) and Masson's trichrome (MT), incubated with antibodies against smooth muscle alpha-actin (alpha-SMA), smooth muscle myosin heavy chain (SMMHC), smoothelin (SM) and histone deacetylase 8 (HDAC8) and processed for TEM. Control specimens exhibited homogeneous immunoreactivity for all antibodies. Diseased specimens showed normal smooth muscle morphology by HE and MT. While anti-alpha-SMA staining was generally normal, immunoreactivity for SMMHC, HDAC8 and/or SM was either absent or focally lacking in Hirschsprung's disease (80%), idiopathic megacolon (75%) and slow-transit constipation (70%). Ultrastructurally, clusters of myocytes with noticeably decreased myofilaments were observed in all diseases. SMMHC and the novel smooth muscle markers SM and HDAC8 often display striking abnormalities linked to the smooth muscle contractile apparatus unnoticed by both routine stainings and alpha-SMA, suggesting specific defects of smooth muscle cells involved in the pathogenesis of gastrointestinal motility disorders.

Actins↗
PubMed1998

A model to investigate postoperative ileus with strain gauge transducers in awake rats.

BACKGROUND: Postoperative ileus influences patients well-being, hospital stay, and health cost, and postoperative inhibition of colonic motility is a major contributor to postoperative ileus. Experimental models for investigating postoperative ileus are needed. In particular, recording of postoperative colonic motility in awake rats has not been described yet. MATERIAL AND METHODS: Gastric, small intestinal, and colonic motility were recorded with strain gauge transducers in awake rats, and the effects of anesthesia and abdominal surgery on gastrointestinal motility were investigated. RESULTS: Ether anesthesia increased gastric motility and inhibited small intestinal motility, while enflurane anesthesia had only minor effects on gastrointestinal motility. Abdominal surgery inhibited gastric, small intestinal, and colonic motility, and a detailed analysis of gastrointestinal motility in our postoperative ileus model is given. CONCLUSIONS: We established a model to record gastric, small intestinal, and colonic motility in awake rats postoperatively. We could demonstrate that enflurane anesthesia had little effect on gastrointestinal motility, while laparotomy and short manipulation of the cecum produced a prolonged inhibition of gastrointestinal motility. Our model could be used to investigate postoperative ileus, particularly of the colon, in awake rats.

Abdomen↗
PubMed1991

[Inhibition of gastric acid secretion normalizes interdigestive motor activity in the stomach in dogs].

Recently, intragastroduodenal acidity has been shown to play an important role in interdigestive gastrointestinal motility. In this study, gastrointestinal motility and intragastric pH changes were monitored simultaneously in dogs, to characterize 1) the relationship between intragastric pH changes and IMC, and 2) the effects of intragastric acidity on motilin-induced phase III contractions in the gastric antrum by using secretagogues and an H2 receptor antagonist (cimetidine). As a result, intragastric pH showed periodic changes with gastric IMC in conscious dogs. Furthermore, motilin-induced gastric phase III contractions were inhibited by gastric acidification. But inhibition of gastric acid secretion by cimetidine normalized both the motor index and migration of the contractions. In conclusion, gastric acid secretion may influence the sensitivity to motilin of the stomach, and play an important role in the regulation of interdigestive gastric motility.

Animals↗
PubMed1983

Effects of emetic and cathartic agents on the gastrointestinal tract and the treatment of toxic ingestion.

Emetic drugs and saline cathartics produce direct or reflex changes in gastrointestinal motility. The changes in gastrointestinal smooth muscle function may be important in the rapid oral or rectal expulsion of gastrointestinal contents, effects which serve as a basis for emetic and cathartic drug use in the treatment of toxic ingestion. Because of difficulties in recording gastrointestinal smooth muscle contractile activity from the intact, unanesthetized animal or man, relatively few studies have attempted to characterize the changes in gastrointestinal motility preceding vomiting. Limited results from past studies and the results of more recent studies employing improved technology suggest that pharmacological activation of the emetic reflex is accompanied by characteristic movements of the stomach and small intestine. The gastric response consists of initial muscle relaxation and an expansion of gastric volume. The intestine responds with a contraction, which begins in the distal ileum and migrates orad over the entire small intestine immediately before active retching. The changes in gastric and intestinal motility may be initiated by structures in the central nervous system and may be an important component of the emetic reflex. This article urges more active research to characterize the gastrointestinal emetic response and to investigate more generally the therapeutic value of emesis in the treatment of toxic ingestion. Emphasis should be placed on the clinically important emetic drugs apomorphine and syrup of ipecac. Studies comparing the efficiency of removal of gastrointestinal contents, resultant blood levels of orally administered drugs with and without emesis, differences in the gastrointestinal emetic response between agents and the pharmacology of the gastrointestinal emetic response should be performed. Studies should also be conducted to determine the pharmacology of the emetic sensory receptors in the gastrointestinal tract and the intraluminal physical-chemical or gastrointestinal physiological factors influencing gastrointestinal emetic sensory receptor activation. The results would demonstrate the value of emesis in various poison cases and help establish criteria for use and selection of emetic drugs. No less experimental attention should be devoted to the cathartic drugs.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1991

[Relations between gastrointestinal interdigestive motility and secretion].

The motility of the upper gastrointestinal tract in the interdigestive state shows a cycling pattern called Migrating Motor Complex (MMC) and is composed by phases I, II and III. Gastric, biliary and pancreatic secretion show cyclical fluctuations during fasting closely associated with the motor activity. The motor and secretory interdigestive activity is regulated by a complex interplay of nerval and humoral mechanisms. Among them, motilin, a gastrointestinal hormone mainly secreted from the duodenum, is supposed to play a central role in the initiation of phase III. Gastric acid secretion, directly or by means of motilin release, may modulate the duration of the MMC and the propagation of phase III in the small intestine. Pancreatic secretion does not initiate phase III but may exert a control on gastric interdigestive motility probably by means of pancreatic polypeptide release. Biliary interdigestive secretion seems to play a little or no role in the control of these phenomena. The coordination of motor and secretory events is likely to be under control of the duodenum.

Animals↗
PubMed1997

The rumination syndrome: clinical and manometric profile, therapy, and long-term outcome.

The aims of this study were to investigate the diagnostic studies necessary to identify rumination syndrome and the long-term therapeutic outcomes of patients with rumination syndrome. Sixteen patients with rumination were evaluated between 1989 and 1995. Esophageal motility, gastric emptying, upper gastrointestinal motility, and electrogastrography of all patients were reviewed; follow-up information about their current status was available from 10 of the 16 patients. Duration of symptoms was 77.2 months and the mean age was 28.5 years at the time of diagnosis. Esophageal and upper gastrointestinal motility, gastric emptying, and electrogastrographic studies were all normal. Mean lower esophageal pressure was 12.7 mm Hg and three of the 16 patients had a decreased pressure of less than 6 mm Hg. Ten patients were followed for a mean duration of 31.2 months. Five of 10 patients used biofeedback and relaxation techniques and reported subjective improvement. Our results indicate that rumination syndrome is often confused with a gastric motility disorder and diagnosis is possible if one is aware of this condition. Although there is not a definitive management protocol for this condition, reassurance and education of the patient and the family are crucial first steps followed by behavioral and relaxation programs.

Adult↗
PubMedDate not supplied

Mesenteric lymph collected during peritonitis or sepsis potently inhibits gastric motility in rats.

Gastrointestinal motility is strongly inhibited during peritonitis or sepsis and proinflammatory cytokines released into mesenteric lymph during an acute gastrointestinal insult mediate systemic responses. We investigated whether mesenteric lymph collected during peritonitis or sepsis inhibits gastric motility and gastric emptying. Mesenteric lymph was collected for 12 hours from three experimental groups: vehicle (saline, 1 ml, intraperitoneally [ip], control lymph), peritonitis (0.5% acetic acid, 1 ml, ip, peritonitis lymph), and sepsis (lipopolysaccharide [LPS], 5 mg/kg, 1 ml, ip, sepsis lymph). Gastric motility and gastric emptying were measured in recipient rats in response to lymph injections into the jugular vein. Quantitative polymerase chain reaction (PCR) for tumor necrosis factor alpha (TNFalpha) gene expression in the jejunum and in lymph cells were measured during sepsis. Mesenteric lymph flow significantly increased during peritonitis or sepsis (lymph flow [ml] per 60 minutes; control 2.45 +/- 0.04; peritonitis 2.67 +/- 0.07; sepsis 3.25 +/- 0.1, p < 0.01 vs. control). Injection of peritonitis or sepsis lymph (1 ml) produced a significant and prolonged inhibition of gastric motility in recipient rats (decrease in intragastric pressure and duration: control lymph -0.14 +/- 0.05 cm H(2)O, 1.89 +/- 1.31 minutes; peritonitis lymph: -0.56 +/- 0.06 cm H(2)O, 9.9 +/- 0.9 minutes; sepsis lymph: -0.51 +/- 0.05 cm H(2)O, 6.9 +/- 0.6 minutes; p < 0.001 vs. control for all comparisons). Gastric emptying was significantly inhibited by continuous infusion of sepsis lymph (3 ml per 60 minutes; gastric emptying: saline 81% +/- 4%; control lymph: 80% +/- 6%; sepsis lymph: 44% +/- 10%; p < 0.001 vs. control). TNFalpha gene expression in the gut wall of the jejunum increased during sepsis over 90-fold within the first 2 hours and decreased continuously thereafter (relative TNFalpha mRNA transcription: basal 1.0 +/- 0.05; LPS 2 hours: 91.9 +/- 2.6, p < 0.001 vs. basal; 12 hours: 24.7 +/- 16.8, not significant [NS]; 24 hours: 7.0 +/- 3.4, NS). In conclusion, mediators in mesenteric lymph, possibly cytokines, may be responsible for the inhibition of gastric motility during peritonitis or sepsis. Because the composition of mesenteric lymph probably reflects the interstitial fluid of the gut wall, monitoring visceral lymph might be an extremely beneficial tool to determine mediators released during impaired gut wall function.

Animals↗
PubMed2006

Nonsteroidal anti-inflammatory drugs induce hypermotilinemia and disturbance of interdigestive migrating contractions in instrumented dogs.

Nonsteroidal anti-inflammatory drugs (NSAIDs) induce gastric ulcers due to inhibition of prostaglandin production. Prostaglandins have an influence on physiological gastrointestinal motility, but the relationships between NSAID-induced gastric ulcer, gastrointestinal motility and motilin are unknown. Fifteen dogs were allocated randomly to three groups in which either gelatin, meloxicam or indomethacin was administered. Fecal occult blood and gastrointestinal motility were monitored continuously for 6 days. In addition, analyses of the plasma motilin concentration, gastrointestinal endoscopy and gastric emptying, and detection of motilin cells were performed. Gastrointestinal motility was disturbed in the indomethacin group, presenting as disappearance of interdigestive migrating contractions (IMCs) 3 days before gastric ulcers were detected. Delayed gastric emptying and hypermotilinemia were observed significantly more often in the indomethacin group compared with the other groups. Motilin cell-crypt/villi ratio in the indomethacin group significantly decreased in the duodenum and jejunum, compared with the other groups. No significant changes in any tests were observed in the meloxicam group, when compared with the gelatin group. These findings suggest that the disturbance of IMCs caused by hypermotilinemia, with changes in motilin cell distribution, and delayed gastric emptying induced by indomethacin may contribute to the development of gastric ulcers.

Animals↗
PubMed1985

Effect of selective and non-selective antimuscarinics on rectosigmoid motility and gastrointestinal transit.

In 12 healthy volunteers, a rectosigmoid motility index (RSMI) was measured when either placebo, 0.5 mg atropine, or 5 mg pirenzepine was given intravenously as a single dose, double-blind, in random order after a control period of 30 min. Compared with the control period, atropine gave a significant decrease of the RSMI during the entire recorded period of 90 min, whereas pirenzepine inhibited RSMI only during the first two 15-min periods. In another series of experiments, gastrointestinal transit was assessed by means of a radiographic marker method. In healthy volunteers, gastrointestinal transit was estimated (n = 20) and gastric secretion was measured (basally and after modified sham feeding; n = 10) during oral medication with placebo, 50 mg pirenzepine twice daily, or 17.5 mg benzilonium bromide twice daily. In 10 of the volunteers gastrointestinal transit was also estimated with 35 mg benzilonium bromide twice daily, and in the other 10 volunteers with 0.6 mg L-hyoscyamine twice daily. The number of retained markers was significantly lower during pirenzepine than during L-hyoscyamine treatment. Neither dose of benzilonium bromide changed the transit of markers. Compared with non-selective antimuscarinics, the effect of pirenzepine was differential: with equipotently acid-reducing doses the decrease of the RSMI after pirenzepine lasted shorter and gastrointestinal transit was accelerated.

Adult↗
PubMed1991

Neuromuscular disease of the gastrointestinal tract.

Gastrointestinal motility is the function of gastrointestinal smooth muscle. It is controlled by both the intrinsic and extrinsic nerves of the gastrointestinal tract and, to a lesser degree, the gastrointestinal hormones. Therefore, any abnormality of the above factors, theoretically, can cause gastrointestinal dysmotility. In a clinical situation, commonly seen is gastrointestinal dysmotility caused by either smooth muscle or intrinsic and extrinsic nerves dysfunction. Diseases that cause smooth muscle dysfunction include familial visceral myopathies, nonfamilial visceral myopathies, collagen disease, muscular dystrophies, amyloidosis, thyroid disease, and so on. Diseases that cause enteric nerve dysfunction include familial visceral neuropathies, nonfamilial visceral neuropathies, diabetes mellitus, Chagas' disease, ganglioneuromatosis of the intestine, visceral neuropathy of carcinomatosis, Parkinson's disease, and so on. The patients with neuromuscular disease of the gastrointestinal tract have a wide range of clinical manifestations regardless of the underlying cause. At one end of the spectrum, the patients may be asymptomatic, and at the other end of the spectrum, the patients may have functional obstruction of the gastrointestinal tract. Plain abdominal x-rays, upper gastrointestinal (UGI) and small bowel x-rays, enteroclysis, barium enema, and manometric studies are useful for the work-up of these patients. Enteroclysis is especially helpful in ruling out mechanical obstruction of the small intestine in patients with chronic intestinal pseudo-obstruction. Treatment is mainly symptomatic and supportive. There is no effective drug to improve gastrointestinal motility. Surgery may be helpful in selected cases of severe gastrointestinal dysmotility.

Gastrointestinal Diseases↗
PubMed1995

Pharmacokinetic considerations in gastrointestinal motor disorders.

Although it has been recognised that alterations in gastrointestinal motility, whether induced by physiological or pathological processes, have significant effects on the pharmacokinetics of orally administered drugs, this subject has received inappropriately little attention. Studies relating to this topic have focused on healthy volunteers and animals and have largely been confined to the effects of single drug doses. There is limited information about the effects of disease on pharmacokinetics under steady-state conditions. Changes in gastrointestinal motility may affect the pharmacokinetics of orally administered drugs by altering the rate of delivery, bioavailability or mucosal absorption of the drug. In general the rate of absorption and time taken to achieve maximal plasma concentrations for well absorbed drugs may be modified by changes in gastrointestinal motility, but overall bioavailability is not usually affected. In these cases the therapeutic and clinical effects of the alteration in pharmacokinetics will, therefore, depend on which parameters are important for the action of the drug. For poorly absorbed drugs both the rate of absorption and bioavailability are likely to be altered by changes in gastrointestinal motility. However, the complex effects of food and disease, as well as the properties and formulation of any drug (solubility, ease of dispersion, delayed release formulation) often make the prediction of the magnitude, or even the direction, of any effect difficult to predict. Drugs with direct effects on gastrointestinal motility may influence their own patterns of absorption. In patients with gastrointestinal motility disorders, drugs administered in a controlled release formulation, or those with poor bioavailability, are most likely to have a poorly predictable therapeutic effect. Care should be taken to ensure that the formulation of the drug, its timing of administration in relation to meals and the use of coadministered drugs optimise, or at least ensure consistent absorption.

Administration, Oral↗
PubMed2005

Nitric oxide synthase inhibition results in immediate postoperative recovery of gastric, small intestinal and colonic motility in awake rats.

BACKGROUND: Nitric oxide (NO) is known to inhibit gastrointestinal motility. However, no detailed analysis of gastric, small intestinal and colonic motor effects, including effects on contraction frequency, has, as yet, been reported after NO inhibition in awake rats. We therefore investigated the effects of NO synthase inhibition on gastric, small intestinal and colonic motility in awake rats under baseline conditions and in a postoperative ileus model. METHODS: In Sprague-Dawley rats, strain gauge transducers were sutured either to the gastric corpus, the small intestine or the colon. After 3 days, L-NMMA (NO synthase inhibitor), D-NMMA or vehicle was given i.v., while the motility was recorded continuously. In addition, postoperative gastric, small intestinal or colonic motility was investigated after L-NMMA or vehicle treatment prior to abdominal surgery. The motility index, the contraction amplitude, the area under the contraction amplitude and the contraction frequency were analysed. RESULTS: L-NMMA decreased gastric motility to 60+/-8% for about 15 min, but continuously increased small intestinal motility to 221+/-22% and colonic motility to 125+/-7% compared to baseline (baseline=100%; p<0.01 for all comparisons). L-NMMA increased the contraction frequency throughout the gastrointestinal tract (stomach, 13+/-2%; small intestine, 8+/-1%; colon, 16+/-5%; p<0.01 vs. baseline for all comparisons). L-NMMA injection prior to surgery did not prohibit intraoperative inhibition of gastrointestinal motility, but did result in immediate recovery of gastric, small intestinal and colonic motility postoperatively (L-NMMA vs. vehicle, 0-60 min postoperatively; stomach, 90+/-9% vs. 53+/-3%; small intestine, 101+/-5% vs. 57+/-3%; colon, 134+/-6% vs. 60+/-5%; p<0.01 for all comparisons; no significant difference between preoperative baseline motility and L-NMMA treated rats postoperatively). CONCLUSIONS: Under baseline conditions, endogenous NO inhibits small intestinal and colonic motility and gastric, small intestinal and colonic contraction frequency in awake rats. In the early postoperative period, endogenous NO is a major inhibitory component that seems to constitute the common final pathway of mediators and the neural pathways inhibiting gastrointestinal motility in rats.

Animals↗
PubMed1994

Epidural anesthesia accelerates the recovery of postischemic bowel motility in the rat.

BACKGROUND: Intestinal ischemia is associated with derangement of gastrointestinal motility. Uncontrolled clinical observations that bupivacaine injected into the epidural space causes faster recovery of bowel motility after various abdominal operations led us to assess the hypothesis that epidural anesthesia can hasten the recovery of gastrointestinal motility in the immediate postischemic period. METHODS: Gut motility studies were performed in rats in which epidural anesthesia and intestinal ischemia could be initiated without the need to provoke surgical trauma. Epidural lidocaine was compared to epidural saline in their effect on intestinal motility after a 30-min period of bowel ischemia. RESULTS: Total ischemia to the small bowel resulted in pronounced postischemic adynamic ileus as evidenced by only 0.7% of the total length of the small bowel filled with a marker meal at the end of the study period (transit index) compared with 84.4% in the control group. Lidocaine epidural anesthesia caused significantly more rapid resolution of the adynamic ileus (60.3% of the bowel filled with the marker meal vs. 30.9% in the controls in which saline was injected). CONCLUSIONS: Epidural lidocaine compared to epidural saline hastens the recovery of gastrointestinal motility in rats after a 30-min period of bowel ischemia. This effect may be elicited by attenuation of sympathetic efferent inhibitory pathways or by vasodilatation caused by the sympathetic block. These results suggest that lidocaine epidural block not only alleviates pain in situations of ischemic injury to the bowel but may also hasten the recovery from postischemic paralytic ileus.

Anesthesia, Epidural↗
PubMed1997

Gastrointestinal motor activity in conscious ferrets.

Gastrointestinal motility was measured with force transducers in conscious ferrets. The gastrointestinal motility pattern in both the interdigestive and digestive states was similar to that reported for humans. The activity front, phase III contractions of the migrating motor complex, occurred cyclically in the antrum and migrated to the duodenum and ileum in the interdigestive state, and relatively low-amplitude contractions were sustained in the antrum, duodenum and ileum in the digestive state. Colonic motility was characterized by basal relatively low-amplitude contractions and a single high-amplitude contraction preceding defecation. Cisapride (0.3-3 mg/kg s.c.) enhanced antral and colonic motility. This ferret model will help the investigation and evaluation of drug effects on gastrointestinal motility in humans.

Animals↗
PubMedDate not supplied

Long-term response to subtotal colectomy in colonic inertia.

The purpose of this study was to determine the long-term outcome of patients who had previously undergone subtotal colectomy for severe idiopathic constipation at the University of Florida between 1983 and 1987. In addition, we aimed to determine whether preoperative motility abnormalities of the upper gastrointestinal tract are more common among those patients who have significant postoperative complications after subtotal colectomy. We evaluated 13 patients who underwent subtotal colectomy for refractory constipation between 1983 and 1987 at the University of Florida. Preoperatively, all patients exhibited a pattern consistent with colonic inertia as demonstrated by means of radiopaque markers. Each patient was asked to quantitate the pain intensity and frequency of their bowel movements before and after surgery. In seven patients an ileosigmoid anastomosis was performed, whereas in six patients an ileorectal anastomosis was used. Abdominal pain decreased after subtotal colectomy. Patients with abnormal upper gastrointestinal motility preoperatively experienced greater postoperative pain than those with normal motility regardless of the type of anastomosis. In addition, the number of postoperative surgeries was similar in those patients with abnormal upper motility compared to those with normal motility. Overall, the total number of bowel movements per week increased from 0.5 +/- 0.03 preoperatively to 15 +/- 4.5 (P < 0.007) postoperatively. The results of our study suggest that patients with isolated colonic inertia have a better long-term outcome from subtotal colectomy than patients with additional upper gastrointestinal motility abnormalities associated with their colonic inertia.

Adolescent↗