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PubMed2002

Purification, characterization, and biological activity of a substance P-related peptide from the gut of the Australian lungfish, Neoceratodus forsteri.

A peptide with mammalian substance P (SP)-like immunoreactivity was isolated from an extract of the spiral intestine of the Australian lungfish, Neoceratodus forsteri. The primary structure of this peptide was established as Lys-Pro-Arg-Pro-Asp-Glu-Phe-Tyr-Gly-Leu-Met . NH2, showing 64% identity with mammalian SP. In isolated preparations of lungfish foregut circular muscle, lungfish SP produced a slow, long-lasting tonic contraction, with a pD2 value of 8.19. Lungfish midgut circular muscle preparations responded to lungfish SP rapidly and in a more complex manner. There was an increase in the frequency of spontaneous activity (pD2 = 8.76), associated with diminished amplitude of the spontaneous contractions (pD2 = 9.24), also coupled in some preparations with a tonic contraction (pD2 = 8.43). The response patterns of foregut and midgut circular muscle to acetylcholine (ACh) were very similar to those seen to lungfish SP. Lungfish SP and ACh, however, had very weak effects on both foregut and midgut longitudinal muscle. These data demonstrate that lungfish SP may be a physiologically important regulator of gastrointestinal motility in Neoceratodus. This study further confirmed that the structures of SP-related peptides have been strongly conserved under the pressure of vertebrate evolution, particularly in preserving the functionally important sequence, Phe-Xaa-Gly-Leu-Met . amide, at the C-terminus. The sequence of lungfish SP is identical to that of bufokinin, a SP-related peptide previously isolated from the intestine of the cane toad, Bufo marinus, supporting the hypothesis that lungfishes and amphibians share a common ancestor.

Acetylcholine↗
PubMed1989

Anesthesia and gastrointestinal surgery.

Anesthesia can have various effects on the outcome of surgery, especially gastrointestinal procedures. Many anesthetic agents, for example, produce a fall in lower esophageal sphincter pressure, which can allow reflux of gastric contents into the lower esophagus. This can lead to potentially fatal aspiration of vomit. Anesthesia also alters gastrointestinal motility, secretion, and absorption; postoperative opiate analgesia in particular contributes to delayed gastric emptying. Anesthetic technique can affect the success of intestinal anastomosis; for example, intravenous induction agents and some inhalational anesthetics decrease regional blood flow, whereas regional anesthetics may act to increase colonic blood flow. Other aspects of anesthetic management are also discussed as they relate to surgical outcome; examples are the use of invasive monitoring in elderly patients, the importance of oxygen delivery to the anastomosis, and the effect of transfusion on survival after surgery for carcinoma.

Anastomosis, Surgical↗
PubMed1997

Advances in the diagnosis and treatment of gastroesophageal reflux disease.

Pathophysiology and treatment of gastroesophageal reflux (GER) in children have often been extrapolated from studies in adult patients. Fortunately, many groups are now addressing GER specifically in relation to children. Abnormalities in gastrointestinal motility are described in gastroesophageal reflux GER, and there are several new studies looking at this issue in infantile GER. An international working group has put together recommendations for management of infantile GER. The results of a large pediatric study using omeprazole and a review of the use of the prokinetic cisapride in pediatrics are summarized. Several papers review recent experiences with laparoscopic fundoplication. New diagnostic modalities used to investigate GER in infants and children are discussed. These studies aid in both our understanding of possible pathogenesis of GER as well as treatment of the young patient with GER.

Child↗
PubMed2005

Spasmogenic activity and acute toxicity of Yumijangquebo, a herbal laxative formulation.

We evaluated the pharmacological properties and spasmogenic activities of Yumijangquebotrade mark, a Korean herbal laxative formulation. Doses in the range 12-50 microg/ml induced a large spasmogenic effect in isolated guinea pig ileum, similar to that induced by acetylcholine. Pre-treating the tissue with atropine (0.2 microM) completely abolished the contractile effect of Yumijangquebo. The spasmogenic effect of Yumijangquebo and the inhibition of this effect by atropine suggest that a cholinergic mechanism is responsible for its effects. Yumijangquebo increased the gastrointestinal motility in ICR mice at doses between 10 and 37 mg/kg. Yumijangquebo exhibited higher activity than three other laxatives tested, which had activities about 85% of that of Yumijangquebo. In an acute toxicity study using Sprague-Dawley rats, the median lethal dose (LD50) of Yumijangquebo was greater than 2000 mg/kg, and we found no pathological changes in macroscopic examination by necropsy of rats treated with Yumijangquebo. We conclude that Yumijangquebo may be safely used as a herbal spasmogenic laxative agent.

Acetylcholine↗
PubMed1995

Effect of motilin on the L-leucine transport in rabbit jejunum.

Motilin is a gastrointestinal peptide that stimulates the gastrointestinal motility in several species. The aim of the present work has been to determine the effect of motilin on the L-leucine absorption in rabbit jejunum. The results show that motilin inhibits the L-leucine Na(+)-dependent system of transport located in the mucosal border mainly by diminishing the apparent Vmax. Motilin did not directly affect the Na(+)-dependent system of transport, but it seems to act across the protein kinase C (PKC). These results suggest that motilin may act as a regulatory hormone of the intestinal absorption of nutrients.

Animals↗
PubMed1987

Gastrointestinal transit rate-related absorption of emepronium: a study in mice.

The gastrointestinal (GI) absorption in mice of the anticholinergic quaternary ammonium compound emepronium, assessed by the urinary excretion of radioactivity and unchanged drug, increased from 1% to 7% and from 0.5% to 5%, respectively, in the dose range 0.1 to 40 mg/kg, whereafter a plateau was reached. Changes in the metabolism were evident at doses exceeding 80 mg/kg when 80% of the radioactivity was excreted as unchanged emepronium, as compared to 50% at lower doses. No dose-dependent urinary excretion of radioactivity was detected following intravenous injection. The increase in the fraction of the dose excreted in the urine after oral administration therefore cannot be easily explained by a dose-dependent metabolism or renal excretion. However, a relationship was seen between the reduced gastrointestinal motility, produced by increasing doses of the drug, and the increased bioavailability. Atropine sulphate given subcutaneously (1-50 mg/kg) more than doubled the urinary recovery of a small pharmacologically inactive oral dose of emepronium (5 mg/kg) and thus confirmed the transit rate-dependent absorption of emepronium. The superimposed effect of the pharmacological action on the GI transit rate, derived from the inherent property of an anticholinergic drug, may be of special significance for a drug with a low degree of absorption and a high variability, such as has been observed in clinical trials with the quaternary drug emepronium (Cetiprin).

Animals↗
PubMed1998

Sympathetic pathways mediate GLP-1 actions in the gastrointestinal tract of the rat.

The aim of this study was to establish the actions of GLP-1 (7-37) on gastrointestinal motility in rats. We prepared anaesthetized Sprague-Dawley rats with strain-gauges in the antrum, duodenum and the proximal jejunum and a catheter in the aorta close to the coeliac artery for close infusion of substances. Intraarterial GLP-1 infusions (3 x 10(-10) and 3 x 10(-9) moles/kg per 10 min) (n = 8) induced inhibition of spontaneous motor activity in the antrum, duodenum and proximal jejunum. Inhibition induced by GLP-1 was reversed by i.v. infusion of GLP-1 receptor antagonist, Exendin (9-39) (3 x 10(-8) moles/kg per 10 min) (n = 6). Neither the presence of L-NNA (10(-5) moles/kg) (n = 9) nor the VIP receptor antagonist [4-Cl-D-Phe6, Leu17]-VIP (3 x 10(-8) moles/kg per 10 min) (n = 8) modified responses to GLP-1. However, a combination of the adrenergic blockers phentolamine and propranolol (1 mg/kg each) (n = 8) completely blocked motor actions of GLP-1 in all the organs studied. Moreover, inhibition of gastrointestinal motor activity by GLP-1 was blocked by previous infusion of hexamethonium (10 mg/kg) (n = 4). This study demonstrates that GLP-1 inhibits gastrointestinal motor activity of the rat acting on specific GLP-1 receptors and via stimulation of adrenergic pathways.

Animals↗
PubMed1997

Safety pharmacology of a combination of tinidazole and oxyphenonium bromide.

The effect of a combination of 150 mg tinidazole (CAS 19387-91-8) and 1 mg oxyphenonium bromide (CAS 50-10-2), referred to as the combination, was examined in various animal species to assess its safety. In mice and rats, the combination in the dose range 30-1000 mg/kg p.o. or 250 mg/kg i.p. did not produce behavioural or neurological changes, nor did it influence pentobarbital sleeping time, though, alcohol sleeping time was altered. In anaesthetised dogs, neither blood pressure, ECG, heart rate, respiration or gastrointestinal motility was affected after single intraduodenal administration of the combination 20 and 50 mg/kg or after chronic oral administration of 25 mg/kg daily for 15 days. In isolated organs, viz. perfused rabbit heart, guinea-pig ileum and rat ileum no significant changes were observed following various doses of the combination, compared to tinidazole and oxyphenonium bromide given alone in corresponding concentrations. In conclusion, the pharmacological profile of the aforementioned combination in the dosages employed in mice, rats, guinea-pigs, rabbits and dogs shows that it is safe and well tolerated.

Animals↗
PubMed1984

M&B 28,767: a potent anti-secretory and anti-ulcer PG analogue. A comparative study with 16, 16' dimethyl PGE2 methylester.

M&B 28,767 [(+/-)11-deoxy-16-phenoxy-omega-tetranor PGE1] and 16, 16'-dimethyl PGE2 methylester (DMPG) were compared for their effects on gastric acid secretion (GAS) and gastric ulceration (GU), employing various laboratory models. In anaesthetised rats, GAS was stimulated by a continuous i.v. infusion of pentagastrin (30 micrograms/kg/h), and PG analogues were perfused through the stomach for 1 h. M&B 28,767 (3-15 micrograms/kg/h) and DMPG (3-60 micrograms/kg/h) reduced GAS in a dose-related manner, the ED50 values being 4 and 15 micrograms/kg/h respectively. In conscious rats possessing indwelling gastric cannulae, oral doses of M&B 28,767 (0.025-0.1 microgram/kg) and DMPG (0.50-1.0 microgram/kg) caused a prolonged inhibition of pentagastrin-stimulated GAS. M&B 28,767 was 17 times more potent than DMPG; the respective ED50 values were 0.036 and 0.6 microgram/kg. Indomethacin-induced ulceration in rats, was reduced by both M&B 28,767 and DMPG; the respective ED50 values being 3.0 and 0.8 micrograms/kg. Both compounds given orally increased gastrointestinal motility in mice; M&B 28,767 (1-3 mg/kg) and DMPG (0.1-0.3 mg/kg) caused diarrhoea, the former being about 0.1 times as potent as the latter. In another test, M&B 28,767 (0.5-5.0 mg/kg) and DMPG (10-40 micrograms/kg) overcame morphine-induced constipation in a dose-related manner, the respective ED50s being 0.9-1.4 mg/kg and 20-40 micrograms/kg. Thus, M&B 28,767 had a better profile of activity than DMPG as an antisecretory and antiulcer agent.

16,16-Dimethylprostaglandin E2↗
PubMedDate not supplied

Reflex gastric motor inhibition caused by intraperitoneal bradykinin: antagonism by Hoe 140, a bradykinin antagonist.

Bradykinin (BK) has been reported to have mixed excitatory/inhibitory effects on gastrointestinal motility. The present study examined the mechanism responsible for the inhibition of gastric motor activity caused by intraperitoneal administration of BK. Gastric motor activity was measured by recording the intragastric pressure (IGP) of phenobarbital-anesthetized rats via a transesophageal catheter. To facilitate the study of inhibitory influences, gastric motility was stimulated by neurokinin A (NKA), which on intravenous injection evoked reproducible gastric contractions as measured by a rise of IGP. Intraperitoneal injection of BK (0.1-10 nmol) inhibited the NKA-induced increase in IGP in a dose-dependent manner, and the effect of epigastric administration of BK was not significantly different from that of intraperitoneal administration. The inhibitory effect of intraperitoneal BK on gastric motility was due to an effect on BK2 receptors because it was blocked by prior intraperitoneal injection of the BK2 antagonist Hoe 140. The specificity of this BK antagonist was demonstrated by its inability to antagonize the effect of intraperitoneal hydrochloric acid (HCl), which, like BK, inhibited the NKA-induced gastric contractions. Because the BK- and HCl-induced inhibition of the NKA-induced rise of IGP was abolished by acute removal of the celiac-superior mesenteric ganglion complex, but left unaltered by acute bilateral subdiaphragmatic vagotomy, it is inferred that intraperitoneal BK inhibits gastric motor activity via activation of an autonomic reflex that involves prevertebral ganglia.

Animals↗
PubMed1998

Effects of cisapride on symptoms and postcibal small-bowel motor function in patients with irritable bowel syndrome.

BACKGROUND: Irritable bowel syndrome is a common cause of abdominal pain and discomfort and may be related to disordered gastrointestinal motility. Our aim was to assess the effects of long-term treatment with a prokinetic agent, cisapride, on postprandial jejunal motility and symptoms in the irritable bowel syndrome (IBS). METHODS: Thirty-eight patients with IBS (constipation-predominant, n = 17; diarrhoea-predominant, n = 21) underwent 24-h ambulatory jejunal manometry before and after 12 week's treatment [cisapride, 5 mg three times daily (n = 19) or placebo (n = 19)]. RESULTS: In diarrhoea-predominant patients significant differences in contraction characteristics were observed between the cisapride and placebo groups. In cisapride-treated diarrhoea-predominant patients the mean contraction amplitude was higher (29.3 +/- 3.2 versus 24.9 +/- 2.6 mm Hg, cisapride versus placebo (P < 0.001); pretreatment, 25.7 +/- 6.0 mm Hg), the mean contraction duration longer (3.4 +/- 0.2 versus 3.0 +/- 0.2 sec, cisapride versus placebo (P < 0.001); pretreatment, 3.1 +/- 0.5 sec), and the mean contraction frequency lower (2.0 +/- 0.2 versus 2.5 +/- 0.4 cont./min, cisapride versus placebo (P < 0.001); pretreatment, 2.5 +/- 1.1 cont./min] than patients treated with placebo. No significant differences in jejunal motility were found in the constipation-predominant IBS group. Symptoms were assessed by using a visual analogue scale before and after treatment. Symptom scores relating to the severity of constipation were lower in cisapride-treated constipation-predominant IBS patients [score, 54 +/- 5 versus 67 +/- 14 mm, cisapride versus placebo (P < 0.05); pretreatment, 62 +/- 19 mm]. Diarrhoea-predominant IBS patients had a higher pain score after cisapride therapy [score, 55 +/- 15 versus 34 +/- 12 mm, cisapride versus placebo (P < 0.05); pretreatment, 67 +/- 19 mm]. CONCLUSION: Cisapride affects jejunal contraction characteristics and some symptoms in IBS.

Adult↗
PubMed1987

Effects of peptide YY (PYY) on mouth to caecum intestinal transit time and on the rate of gastric emptying in healthy volunteers.

The effect of an infusion of two doses of peptide YY (PYY), a novel putative gastrointestinal hormone, has been assessed on mouth to caecum intestinal transit time and on the rate of gastric emptying after ingestion of an inert 200 ml liquid meal thought unlikely to interrupt fasting gastrointestinal motility patterns. A low dose of PYY was chosen to give plasma concentrations within the range seen postprandially in healthy subjects, while the high dose mimicked the raised levels seen in several malabsorptive conditions. During infusion of PYY at 0.18 pmol/kg/min plasma concentrations rose from a basal of 8 +/- 2 pmol/l to 38 +/- 5 pmol/l and at 0.51 pmol/kg/min to 87 +/- 10 pmol/l. Mouth to caecum transit time was delayed from 67 +/- 4 mins on the saline infusion day to 94 +/- 7 mins (p less than 0.01) on the low dose and 192 +/- 9 mins (p less than 0.001) on the high dose infusion day. Time to 50% gastric emptying was prolonged from 37 +/- 8 mins during saline infusion to 63 +/- 10 mins (p less than 0.05) during low and 130 +/- 12 mins (p less than 0.001) during high dose infusion. Thus the infusion of PYY shows a dose related inhibition of mouth to caecum intestinal transit time and of the rate of gastric emptying and suggests this novel hormonal peptide to be of importance in gastrointestinal physiology.

Dose-Response Relationship, Drug↗
PubMed1997

Gabapentin (neurontin) and S-(+)-3-isobutylgaba represent a novel class of selective antihyperalgesic agents.

1. Gabapentin (neurontin) is a novel antiepileptic agent that binds to the alpha 2 delta subunit of voltage-dependent calcium channels. The only other compound known to possess affinity for this recognition site is the (S)-(+)-enantiomer of 3-isobutylgaba. However, the corresponding (R)-(-)-enantiomer is 10 fold weaker. The present study evaluates the activity of gabapentin and the two enantiomers of 3-isobutylgaba in formalin and carrageenan-induced inflammatory pain models. 2. In the rat formalin test, S-(+)-3-isobutylgaba (1-100 mg kg-1) and gabapentin (10-300 mg kg-1) dose-dependently inhibited the late phase of the nociceptive response with respective minimum effective doses (MED) of 10 and 30 mg kg-1, s.c. This antihyperalgesic action of gabapentin was insensitive to naloxone (0.1-10.0 mg kg-1, s.c.). In contrast, the R-(-)-enantiomer of 3-isobutylgaba (1-100 mg kg-1) produced a modest inhibition of the late phase at the highest dose of 100 mg kg-1. However, none of the compounds showed any effect during the early phase of the response. 3. The s.c. administration of either S-(+)-3-isobutylgaba (1-30 mg kg-1) or gabapentin (10-100 mg kg-1), after the development of peak carrageenan-induced thermal hyperalgesia, dose-dependently antagonized the maintenance of this response with MED of 3 and 30 mg kg-1, respectively. Similar administration of the two compounds also blocked maintenance of carrageenan-induced mechanical hyperalgesia with MED of 3 and 10 mg kg-1, respectively. In contrast, R-(-)-3-isobutylgaba failed to show any effect in the two hyperalgesia models. 4. The intrathecal administration of gabapentin dose-dependently (1-100 micrograms/animal) blocked carrageenan-induced mechanical hyperalgesia. In contrast, administration of similar doses of gabapentin into the inflamed paw was ineffective at blocking this response. 5. Unlike morphine, the repeated administration of gabapentin (100 mg kg-1 at start and culminating to 400 mg kg-1) over 6 days did not lead to the induction of tolerance to its antihyperalgesic action in the formalin test. Furthermore, the morphine tolerance did not cross generalize to gabapentin. The s.c. administration of gabapentin (10-300 mg kg-1), R-(-) (3-100 mg kg-1) or S-(+)-3-isobutylgaba (3-100 mg kg-1) failed to inhibit gastrointestinal motility, as measured by the charcoal meal test in the rat. Moreover, the three compounds (1-100 mg kg-1, s.c.) did not generalize to the morphine discriminative stimulus. Gabapentin (30-300 mg kg-1) and S-(+)-isobutylgaba (1-100 mg kg-1) showed sedative/ataxic properties only at the highest dose tested in the rota-rod apparatus. 6. Gabapentin (30-300 mg kg-1, s.c.) failed to show an antinociceptive action in transient pain models. It is concluded that gabapentin represents a novel class of antihyperalgesic agents.

Acetates↗
PubMed1997

Review and analysis of the effects of olestra, a dietary fat substitute, on gastrointestinal function and symptoms.

Olestra, a dietary fat substitute, was recently made available to consumers in savory snacks in three cities. Early reports of gastrointestinal complaints attributed to olestra attracted media coverage and fostered confusion among physicians and consumers about the nature of olestra and its effects on the digestive system. We reviewed all published studies of olestra's gastrointestinal effects and all relevant unpublished studies submitted to the Food and Drug Administration. Each study was analyzed by a group of expert gastroenterologists and epidemiologists. The symptoms reported with olestra ingestion are similar to those reported with ingestion of fiber and sorbitol, although the mechanisms involved in changing stool characteristics differ among these food additives. Olestra's effects on stool habit and characteristics are due to its presence in the stool. Large amounts are more likely to induce gastrointestinal symptoms than small amounts. There is no evidence that olestra induces pathological change in bowel function: there is no increased fluid or electrolyte nor is there altered gastrointestinal motility or microflora. Olestra and triglyceride ingestion resulted in a similar frequency of symptoms in normal adults and children and in people with chronic inflammatory bowel disease in remission. Olestra traverses the digestive tract intact to become a stool additive. Some subjects develop a change in bowel habit and stool characteristics due to the presence of more olestra in the stool. These changes resemble those associated with ingestion of sorbitol and fiber.

Controlled Clinical Trials as Topic↗
PubMed2001

Expression of dystrophin in the mouse myenteric neurones.

Dystrophin, a membrane-associated protein, plays relevant roles in cell functions. Its lack or trunkated expression results in Duchenne muscular dystrophy (DMD), a pathology associated with alterations in gastrointestinal motility considered to be neural in origin. No data are available on the presence of dystrophin in myenteric neurones. We labelled mouse myenteric neurones with DYS1-, DYS2-, DYS3-antibodies; staining was located on the perikarya and processes, with no differences in distribution or intensity among the antibodies; the western immunoblot analysis indicated that myenteric neurones express several dystrophin isoforms; anti-dystrophins/anti-neuronal specific enolase double-labeling confirmed that all neurones express dystrophin. Dystrophin in myenteric neurones might play a role in cytoskeletal organization, axonal transport and signal pathways; its lack might cause the intestinal motor abnormalities reported in DMD patients.

Animals↗
PubMed2005

Pharmacological studies of anti-diarrhoeal activity of Gentianopsis paludosa.

The pharmacological studies of anti-diarrhoeal activity of Gentianopsis paludosa were carried out. The 75% ethanol extract (100-400 mg/kg) of Gentianopsis paludosa inhibited castor oil-induced diarrhoea and also reduced gastrointestinal motility in the charcoal meal test in mice. In the rabbit-isolated ileum, the extract showed inhibitory effects not only on its spontaneous contraction, but also on acetylcholine (Ach, 0.1 mM)- and KCl (60 mM)-induced contractions. Furthermore, the ethanol extract (0.4-0.6 mg/ml) shifted the CaCl2 dose-effect curves to the right in a non-competitive manner and significantly reduced the acetylcholine-induced contraction of isolated ileum in Ca2+-free solution like verapamil (0.1 mM), which suggest that the extract interferes with Ca2+ movement. These results support the traditional use of Gentianopsis paludosa in the treatment of diarrhoea.

Acetylcholine↗
PubMed2006

Gender, age, society, culture, and the patient's perspective in the functional gastrointestinal disorders.

Patients with functional gastrointestinal disorders (FGID) often experience emotional distress, a perceived lack of validation, and an unsatisfactory experience with health care providers. A health care provider can provide the patient with a framework in which to understand and legitimize their symptoms, remove self-doubt or blame, and identify factors that contribute to symptoms that the patient can influence or control. This framework can be strengthened with the consideration of various important factors that impact FGID but are often overlooked. These include gender, age, society, culture, and the patient's perspective. There is evidence for sex- and gender-related differences in FGID, particularly irritable bowel syndrome (IBS). Whereas the majority of FGID, including IBS, bloating, constipation, chronic functional abdominal pain, and pelvic floor dysfunction, are more prevalent in women than men, functional esophageal and gastroduodenal disorders do not appear to vary by gender. Limited studies suggest that sex differences in visceral perception, cardioautonomic responses, gastrointestinal motility, and brain activation patterns to visceral stimuli exist in IBS. Gender differences in social factors, psychological symptoms, and response to psychological treatments have not been adequately studied. However, there appears to be a greater clinical response to serotonergic agents developed for IBS in women compared to men. The impact of social and cultural factors on the meaning, expression, and course of FGID are important. The prevalence of IBS appears to be lower in non-Western than Western countries. Although further studies are needed, the existing literature suggests that they are important to consider from both research and clinical perspectives.

Age Factors↗
PubMed2001

Physiology and pathophysiology of the interstitial cell of Cajal: from bench to bedside. III. Interaction of interstitial cells of Cajal with neuromediators: an interim assessment.

Interstitial cells of Cajal (ICC) control gastrointestinal motility; some pace slow waves and others act in enteric neurotransmission. This review asks the question, does either class of ICC receive and respond to messages carried by neuromediators from these nerves? Relevant evidence includes the presence of receptors or responses to exogenous neuromediators and responses to endogenous neuromediators. Some pacemaking ICC networks have receptors for or respond to some exogenous neuromediators. None is known to respond to endogenous neuromediators. Intramuscular ICC have receptors for and respond to some neuromediators and are required in mice for responses to the exogenous and endogenous neuromediators nitric oxide and acetylcholine. The mechanisms underlying this requirement remain unclear. ICC pathologies exist, but their origins are unknown.

Acetylcholine↗