Статті в журналах: "Gastrointestinal system Motility"

1

Wood, Jackie D. "Enteric Nervous System: Neuropathic Gastrointestinal Motility." Digestive Diseases and Sciences 61, no. 7 (May 3, 2016): 1803–16. http://dx.doi.org/10.1007/s10620-016-4183-5.

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BURKS, THOMAS F. "Central Nervous System Regulation of Gastrointestinal Motility." Annals of the New York Academy of Sciences 597, no. 1 Neurobiology (July 1990): 36–42. http://dx.doi.org/10.1111/j.1749-6632.1990.tb16156.x.

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Alqudah, M., O. Al-Shboul, A. Al-Dwairi, D. G. Al-U´Dat, and A. Alqudah. "Progesterone Inhibitory Role on Gastrointestinal Motility." Physiological Research, no. 2 (April 30, 2022): 193–98. http://dx.doi.org/10.33549/physiolres.934824.

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Progesterone is a steroidal hormone that is produced from the corpus luteum of the ovaries and from the placenta. The main function of progesterone is to promote the secretory differentiation in the endometrium of the uterus and to maintain pregnancy by inhibiting uterine contractions throughout pregnancy. Progesterone performs its actions by activating the classical progesterone nuclear receptors that affect gene transcription and by the non-classical activation of cell surface membrane receptors that accounts for the rapid actions of progesterone. Besides the reproductive roles of progesterone, it exerts functions in many tissues and systems such as the nervous system, the bone, the vascular system, and the gastrointestinal (GI) tract. This review will summarize the recent literature that investigated the role of progesterone in GI tract motility. Most literature indicates that progesterone exerts an inhibitory role on gut smooth muscle cells in part by elevating nitric oxide synthesis, which induces relaxation in smooth muscle. Moreover, progesterone inhibits the signaling pathways that lead to contraction such as Rho kinase inhibition. These data serve as a quick resource for the future directions of progesterone research that could lead to better understanding and more effective treatment of gender-related GI tract motility disorders.

4

Wang, Po-Min, Genia Dubrovsky, James C. Y. Dunn, Yi-Kai Lo, and Wentai Liu. "A Wireless Implantable System for Facilitating Gastrointestinal Motility." Micromachines 10, no. 8 (August 9, 2019): 525. http://dx.doi.org/10.3390/mi10080525.

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Gastrointestinal (GI) electrical stimulation has been shown in several studies to be a potential treatment option for GI motility disorders. Despite the promising preliminary research progress, however, its clinical applicability and usability are still unknown and limited due to the lack of a miniaturized versatile implantable stimulator supporting the investigation of effective stimulation patterns for facilitating GI dysmotility. In this paper, we present a wireless implantable GI modulation system to fill this technology gap. The system consists of a wireless extraluminal gastrointestinal modulation device (EGMD) performing GI electrical stimulation, and a rendezvous device (RD) and a custom-made graphical user interface (GUI) outside the body to wirelessly power and configure the EGMD to provide the desired stimuli for modulating GI smooth muscle activities. The system prototype was validated in bench-top and in vivo tests. The GI modulation system demonstrated its potential for facilitating intestinal transit in the preliminary in vivo chronic study using porcine models.

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Lee, Yunna, Jeongbin Jo, Hae Young Chung, Charalabos Pothoulakis, and Eunok Im. "Endocannabinoids in the gastrointestinal tract." American Journal of Physiology-Gastrointestinal and Liver Physiology 311, no. 4 (October 1, 2016): G655—G666. http://dx.doi.org/10.1152/ajpgi.00294.2015.

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The endocannabinoid system mainly consists of endogenously produced cannabinoids (endocannabinoids) and two G protein-coupled receptors (GPCRs), cannabinoid receptors 1 and 2 (CB1 and CB2). This system also includes enzymes responsible for the synthesis and degradation of endocannabinoids and molecules required for the uptake and transport of endocannabinoids. In addition, endocannabinoid-related lipid mediators and other putative endocannabinoid receptors, such as transient receptor potential channels and other GPCRs, have been identified. Accumulating evidence indicates that the endocannabinoid system is a key modulator of gastrointestinal physiology, influencing satiety, emesis, immune function, mucosal integrity, motility, secretion, and visceral sensation. In light of therapeutic benefits of herbal and synthetic cannabinoids, the vast potential of the endocannabinoid system for the treatment of gastrointestinal diseases has been demonstrated. This review focuses on the role of the endocannabinoid system in gut homeostasis and in the pathogenesis of intestinal disorders associated with intestinal motility, inflammation, and cancer. Finally, links between gut microorganisms and the endocannabinoid system are briefly discussed.

6

Plourde, Victor. "Stress-Induced Changes in the Gastrointestinal Motor System." Canadian Journal of Gastroenterology 13, suppl a (1999): 26A—31A. http://dx.doi.org/10.1155/1999/320626.

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Several autonomic, hormonal, behavioural and neuropeptidergic bodily responses to stressful stimuli have been described over the past few decades. Both animal models and human paradigms have been explored. It is acknowledged that stress modulates gastrointestinal (GI) motility through central mechanisms including corticotropin-releasing-factor. This process requires the integrity of autonomic neural pathways. It has become evident that the effects of stress on GI motility vary according to the stressful stimulus, its intensity, the animal species under study and the time course of the study. Recent evidence suggests that chronic or possibly permanent changes develop in enteric smooth muscle properties in response to stress. In animals, the most consistent findings include retardation of gastric emptying in response to various stressors; acceleration of gastric emptying upon cold stress, presumably through the secretion of brain thyroglobulin-hormone; acceleration of intestinal transit; and stimulation of colonic transit and fecal output. In humans, the cold water immersion test has been associated with an inhibition of gastric emptying, while labyrinthine stimulation induces the transition from postprandial to fasting motor patterns in the stomach and the small bowel. Psychological stress has been shown to induce a reduction in the number and amplitude of intestinal migrating motor complexes and to neither affect nor stimulate colonic motility. These various responses to stress are presumably attributed to the preferential activation of specific neuronal pathways under the influence of a given stimulus or its intensity. The significance of these findings and the directions of further studies are discussed.

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Stern, H. Patrick, Suzanne E. Stroh, Stephen C. Fiedorek, Kelly Kelleher, Michael W. Mellon, Sandra K. Pope, and Phillip L. Rayford. "Increased Plasma Levels of Pancreatic Polypeptide and Decreased Plasma Levels of Motilin in Encopretic Children." Pediatrics 96, no. 1 (July 1, 1995): 111–17. http://dx.doi.org/10.1542/peds.96.1.111.

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Objective. Abnormalities of hormones affecting gastrointestinal motility have been found in "functional" disorders of the gastrointestinal system in adults. One such disorder of childhood, encopresis, is frequently associated with constipation, the treatment of which often eliminates the soiling. We hypothesized that hormones affecting gastrointestinal motility were different between encopretic patients and matched controls. Methods. Ten encopretic patients were matched by age, race, and sex with controls who had no history of encopresis or constipation. After an overnight fast, each child consumed a meal of Ensure, the amount of which was based on body weight. Plasma levels of gastrin, pancreatic polypeptide, cholecystokinin, motilin, thyroxine, estrogen, and insulin were measured 20 and 5 minutes before the meal, and 5, 10, 15, 30, 45, 60, 90, 120, 150, and 180 minutes after the meal. Results. Postprandial levels of pancreatic polypeptide remained consistently higher and peaked earlier (P < .05) for encopretic patients. The motilin response was lower (P < .03) for encopretic children than for controls. Conclusions. We conclude that pancreatic polypeptide and motilin responses to a meal are different in encopretic children than in children in the control group. These gastrointestinal hormone findings may in part explain and/or be the result of the severe constipation that frequently underlies the fecal soiling found in these patients. These findings also suggest the motility of the stomach and small intestine may be abnormal in encopresis.

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Milla, PJ. "Acquired Motility Disorders in Childhood." Canadian Journal of Gastroenterology 13, suppl a (1999): 76A—84A. http://dx.doi.org/10.1155/1999/610486.

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Acquired motility disorders in childhood cause a number of gastrointestinal symptoms – principally, recurrent vomiting, abdominal pain and distension, constipation and loose stools. Gastrointestinal motility disorders result from disturbances of the control mechanisms of gut motor activity, which may be produced by organic disease involving enteric nerves and muscle, perturbation of the humoral environment of the nerves and muscle, and altered central nervous system input. In children, both congenital and acquired disease processes may produce these pathogenetic mechanisms, resulting in syndromes that vary in severity from chronic intestinal pseudo-obstruction to the irritable bowel syndrome.

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Pan, H. L., Z. B. Zeisse, and J. C. Longhurst. "Mechanical stimulation is not responsible for activation of gastrointestinal afferents during ischemia." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 1 (January 1, 1997): H99—H106. http://dx.doi.org/10.1152/ajpheart.1997.272.1.h99.

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Abdominal ischemia reflexly excites the cardiovascular system through activation of visceral sympathetic afferents. Although a number of ischemic metabolites are known to stimulate sympathetic afferents, the contribution of mechanical stimulation to activation of afferents during abdominal ischemia remains uncertain. Thus the present study examined the role of changes in motility in activation of gastrointestinal afferents during ischemia. Single-unit activity of C fiber afferents located on the stomach, duodenum, jejunum, or colon was recorded from the right sympathetic chain of anesthetized cats during 15 min of ischemia. Intraluminal pressure, as a reflection of local mechanical activity, was measured by an open catheter placed in the lumen of the gastrointestinal tract. The results show that gastrointestinal motility was mainly inhibited during abdominal ischemia. Changes in intraluminal pressure did not correlate with afferent discharge activity during ischemia (r = -0.32, n = 10). Furthermore, discharge frequency of gastrointestinal afferents during ischemia was not altered significantly by topical application of 100 micrograms/ml of atropine (3.98 +/- 0.62 to 3.83 +/- 0.59 imp/s, n = 12), which profoundly inhibited local gastrointestinal motility. Collectively, these data indicate that gastrointestinal motility changes during abdominal ischemia do not contribute to activation of gastrointestinal sympathetic C fiber afferents.

10

Spencer, Nick J., and Hongzhen Hu. "Enteric nervous system: sensory transduction, neural circuits and gastrointestinal motility." Nature Reviews Gastroenterology & Hepatology 17, no. 6 (March 9, 2020): 338–51. http://dx.doi.org/10.1038/s41575-020-0271-2.

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11

Nakamura, Hiroyuki, Tadashi Asano, Koichi Haruta, and Keisuke Takeda. "Gastrointestinal motor inhibition by exogenous human, salmon, and eel calcitonin in conscious dogs." Canadian Journal of Physiology and Pharmacology 73, no. 1 (January 1, 1995): 43–49. http://dx.doi.org/10.1139/y95-006.

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Effects of synthetic eel (E-), salmon (S-), and human (H-) calcitonin (CT) on gastrointestinal motility were studied in conscious beagle dogs, which had been implanted with strain gauge force transducers. Intramuscular administration of E-, S-, or H-CT interrupted gastric migrating motor complexes, digestive pattern, and gastric emptying. The order of potency was E-CT = S-CT > H-CT. Motor inhibition induced by CT occurred independently of plasma immunoreactive motilin levels or hypocalcemia. In addition, E-CT and S-CT induced vomiting without a retrograde giant contraction (RGC) during the postprandial state. Apomorphine or CuSO4initiated RGC prior to vomiting. RGC induced by apomorphine was inhibited by pretreatment with E-CT as well as hexamethonium, atropine, or surgical vagotomy. E-CT showed no inhibitory effect on nicotine stimulated contraction of isolated guinea-pig ileum. These results suggest that peripherally administered CT inhibits canine gastrointestinal motility at the central nervous system level by lowering vagal activity.Key words: gastric emptying, motilin, retrograde giant contraction, vagus, vomiting.

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., Manojkumar, and Sangeeta Gehlot. "EFFECT OF SHARAPUNKHA (TEPHROSIA PURPUREA) ON GASTROINTESTINAL SYSTEM." International Journal of Research in Ayurveda and Pharmacy 11, no. 5 (October 30, 2020): 60–63. http://dx.doi.org/10.7897/2277-4343.1105142.

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Sharapunkha (Tephrosia purpurea) is one of the important drugs in Ayurvedic system of medicine. The present study was undertaken to find out the action of Sharapunkha (Tephrosia purpurea) on Gastrointestinal System. During the passage of drug through oral route, it is probable that the active principle present in Sharapunkha, might act on gastrointestinal System. Albino rats were used in this study and divided into control and drug treated group. Drug treated group rats were feed with intragastric drug decoction, along with their normal water and food. Water intake, diet intake, weight of rats, gastrointestinal motility and serum bilirubin level were compared. Healthy human volunteers were selected, and prepared drug decoction was given for 7 days. Observations were done based on self-assessment of the volunteers about any significant physiological variation specially related to the G.I. System. After study, it was found that Sharapunkha enhances intestinal motility, decreases serum bilirubin in albino rats. Human volunteers had feeling of increase appetite, easy bowel motion and increase urge for micturition. These facts suggest that some ingredients of Sharapunkha are acting on the smooth muscles of the bowel and urinary bladder. So, it may be presumed that Sharapunkha influences the feeding and satiety center located in hypothalamus. Sharapunkha decoction preparation does influence the activity of the autonomic nervous system with consequent alterations in the functions of gastrointestinal tract and possibly the urinary system.

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Nors, Jesper, Mette Winther Klinge, Thorbjørn Sommer, Søren Laurberg, Klaus Krogh, and Jonas Amstrup Funder. "Assessment of postoperative gastrointestinal motility in colorectal surgery: a study with the Motilis 3D-transit system." BMJ Innovations 7, no. 1 (November 25, 2020): 53–60. http://dx.doi.org/10.1136/bmjinnov-2019-000396.

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PurposePostoperative recovery following colorectal surgery remains impaired by severe complications including postoperative ileus (POI). Human studies of POI have been limited by a lack of safe and easy-to-use objective methods. Motilis 3D-transit is a completely ambulatory, minimally invasive system whereby electromagnetic capsules are followed by external sensors during their passage of the gastrointestinal (GI) tract. The aim of this study was to evaluate the applicability of the 3D-transit system in a surgical setting.MethodWe included 12 patients as a substudy of the randomised double blind controlled Stimulation of the Autonomic Nervous System In Colorectal Surgery by perioperative nutrition (SANICS)-II trial undergoing elective segmental colonic resection with primary anastomosis at Aarhus University Hospital and Randers Regional Hospital, Denmark. To study region-specific motility, three electromagnetic capsules were administered. One was taken 3 hours before surgery, the next was taken 1 hour before surgery, while the third was placed distal to the anastomosis during surgery. Total and regional GI transit times as well as time until first propulsive colonic contraction were determined.ResultsAll patients tolerated the setup well with no adverse events related to the 3D-transit system. Large variations were found in total GI transit time (26.7–127.6 hours), gastric emptying (0.07–>106.9 hours), small intestinal (1.2–58.4 hours) and colorectal transit time (14.3–>118.1 hours). Time from end of surgery to first propulsive movement in the colon varied from 3.9 to 85 hours. No correlation was found between parameters of GI motility and tolerance of an oral diet or recovery of bowel function.ConclusionThe 3D-transit system allows safe assessment of GI motility in patients operated with segmental colonic resections and primary anastomosis for colorectal cancer. Postsurgical motility varies significantly between patients.

14

Wang, Hao, Wen-Jian Liu, Meng-Jie Hu, Meng-Ting Zhang, and Guo-Ming Shen. "Acupuncture at Gastric Back-Shu and Front-Mu Acupoints Enhances Gastric Motility via the Inhibition of the Glutamatergic System in the Hippocampus." Evidence-Based Complementary and Alternative Medicine 2020 (March 10, 2020): 1–10. http://dx.doi.org/10.1155/2020/3524641.

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Acupuncture strongly alleviates gastrointestinal symptoms and especially promotes gastrointestinal motility. However, the mechanism underlying these processes is poorly understood. This study was designed to examine the effect of electroacupuncture (EA) at gastric back-shu (BL21) and front-mu (RN12) acupoints on gastric motility in functional dyspepsia (FD) rats and to investigate the mechanisms of its effects on the glutamatergic system in the hippocampus. We found that EA at RN12 or BL21 enhanced gastric motility in FD rats, whereas EA at the combination of RN12 and BL21 showed an additional effect. Microdialysis combined with HPLC showed that EA reduced the glutamate content in the hippocampus, and the NMDAR-NO-cGMP signalling pathway was downregulated, as determined by Western blot assays, in FD rats. In addition, we found that decreased gastric motility was significantly restored by the hippocampal infusion of an NMDAR, nNOS, or sGC antagonist. Interestingly, EA had no further effects on gastric motility in the presence of these antagonists in FD rats. Taken together, these results suggest that the hippocampal glutamatergic system is involved in the regulation of gastric motility by EA at RN12 and BL21.

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Krantis, Anthony. "GABA in the Mammalian Enteric Nervous System." Physiology 15, no. 6 (December 2000): 284–90. http://dx.doi.org/10.1152/physiologyonline.2000.15.6.284.

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γ-Aminobutyric acid (GABA) is a transmitter of enteric interneurons, targeting excitatory GABAA or inhibitory GABAB receptors that modulate motility and mucosal function. Enteric GABA may also subserve hormonal and paracrine signaling. Disruption in gastrointestinal function following perturbation of enteric GABA receptors presents potential new target sites for drug development.

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Barone, Joseph A., Lois M. Jessen, John L. Colaizzi, and Robert H. Bierman. "Cisapride: A Gastrointestinal Prokinetic Drug." Annals of Pharmacotherapy 28, no. 4 (April 1994): 488–500. http://dx.doi.org/10.1177/106002809402800413.

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OBJECTIVE: To summarize the pharmacology, pharmacokinetics, efficacy, and safety of cisapride, and to evaluate its potential therapeutic role. DATA SOURCES: A computerized search of the MEDLINE database was used to identify English-language publications of cisapride data in humans. The MEDLINE search was supplemented by review article bibliographies. There was no attempt to limit the search to a specific gastrointestinal motility disorder. STUDY SELECTION: The MEDLINE search alone identified 165 citations. Because of the volume of available human cisapride data, the focus of the efficacy section is on complete published reports of controlled clinical studies. Abstracts and uncontrolled data are discussed only when other information is unavailable to address important aspects. DATA EXTRACTION: Information regarding study design, study population, results, and safety was recorded from each publication. The placebo response to gastrointestinal complaints in patients with motility disorders is high. Therefore, objective evidence of improvement was emphasized when documentation was available. DATA SYNTHESIS: Cisapride stimulates the motility of smooth muscle lining the esophagus, stomach, small intestine, and colon, and increases the tone of gut sphincters in vitro and in vivo. In controlled investigations, cisapride was superior to placebo in relieving symptoms associated with reflux esophagitis, nonulcer dyspepsia, and gastroparesis. Similar symptom and healing effects were observed with cisapride and histamine (H)2-antagonists in reflux esophagitis. Cisapride was either equal to or superior to metoclopramidein relieving reflux symptoms. However, metoclopramide was associated with significantly more central nervous system adverse effects. Cisapride was well tolerated, with adverse effects limited primarily to the gastrointestinal tract. CONCLUSIONS: Cisapride represents an attractive alternative to metoclopramidefor the treatment of a variety of motility disorders. Because it addresses a primary underlying cause of reflux esophagitis, cisapride may also prove to be an effective alternative to acid suppressants in the management of this disorder.

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Sobol, Constantin V. "Stimulatory Effect of Lactobacillus Metabolites on Colonic Contractions in Newborn Rats." International Journal of Molecular Sciences 24, no. 1 (December 30, 2022): 662. http://dx.doi.org/10.3390/ijms24010662.

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Microbiota are known to play an important role in gastrointestinal physiology and pathophysiology. Microbiota and their metabolites can affect gut motility, neural regulation and the enteric endocrine systems and immune systems of the gut. The use of fermented/hydrolyzed products may be a promising new avenue for stimulating gastrointestinal motility. The purpose of this study was to investigate the effect of lactobacillus metabolites (PP), produced using a U.S.-patented fermentation method, on rat colon motility in vitro. The distal colon was incised from newborn male Wistar rats. A sensitive tensometric method for the study of colon contractions was used. The [Ca2+]i in colon tissue was registered using a computerized ratiometric system for an intracellular ion content assay (Intracellular Imaging and Photometry System, Intracellular imaging, Inc. Cincinnati, OH, USA). The cumulative addition of PP induced contraction with sigmoid dose responses with ED50 = 0.13 ± 0.02% (n = 4), where 10% PP was accepted as a maximal dose. This contraction was accompanied by an increase in the concentration of [Ca2+]i. It was shown that introducing Lactobacillus metabolites produced using a U.S.-patented fermentation method quickly stimulates dose-dependent colon contractions and an increase in intracellular calcium. The direct application of PP via enema to the colon could stimulate colon motility and suppress pathogenic microbiota, owing to the antagonistic property of PP on pathogens.

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Idrizaj, Eglantina, Rachele Garella, Roberta Squecco, and Maria Caterina Baccari. "Adipocytes-released Peptides Involved in the Control of Gastrointestinal Motility." Current Protein & Peptide Science 20, no. 6 (May 20, 2019): 614–29. http://dx.doi.org/10.2174/1389203720666190121115356.

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The present review focuses on adipocytes-released peptides known to be involved in the control of gastrointestinal motility, acting both centrally and peripherally. Thus, four peptides have been taken into account: leptin, adiponectin, nesfatin-1, and apelin. The discussion of the related physiological or pathophysiological roles, based on the most recent findings, is intended to underlie the close interactions among adipose tissue, central nervous system, and gastrointestinal tract. The better understanding of this complex network, as gastrointestinal motor responses represent peripheral signals involved in the regulation of food intake through the gut-brain axis, may also furnish a cue for the development of either novel therapeutic approaches in the treatment of obesity and eating disorders or potential diagnostic tools.

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Baldrick, P., D. G. Bamford, and M. L. Tattersall. "An assessment of two gastric transport models currently used in safety pharmacology testing." Human & Experimental Toxicology 17, no. 1 (January 1998): 1–7. http://dx.doi.org/10.1177/096032719801700101.

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1 The potential effects of new drugs on the digestive system can be examined in a number of model systems of which intestinal motility in the mouse and/or gastric emptying in the rat are examples recommended for safety pharmacology evaluation. 2 Intestinal motility, assessed by the transit of carmine dye in the mouse and gastric motility, assessed by stomach weight in the rat, were examined using a range of clinical drugs or potent pharmacological agents known to affect gastrointestinal function. Assessment of both models in the guinea-pig was also evaluated. 3 Activity was demonstrated with codeine, diazepam, atropine and CCK-8 (all of which inhibited gastric function). However, neither model gave consistent and reliable results with the remaining reference compounds, namely metoclopramide, bethanechol, cisa-pride, deoxycholate, carbachol and domperidone. 4 In conclusion, this investigation questions the usefulness of simple models of gastrointestinal transport in the rodent as a means of detecting potential effects of a new drug on the digestive system. This finding should be of concern to the pharmaceutical industry as these simple models are routinely used as part of a regulatory safety pharmacology `package' of studies.

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DiCello, Jesse J., Simona E. Carbone, Ayame Saito, Vi Pham, Agata Szymaszkiewicz, Arisbel B. Gondin, Sadia Alvi, et al. "Positive allosteric modulation of endogenous delta opioid receptor signaling in the enteric nervous system is a potential treatment for gastrointestinal motility disorders." American Journal of Physiology-Gastrointestinal and Liver Physiology 322, no. 1 (January 1, 2022): G66—G78. http://dx.doi.org/10.1152/ajpgi.00297.2021.

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This study assesses the use of positive allosteric modulation as a pharmacological approach to enhance opioid receptor signaling in the enteric nervous system. We demonstrate that selective modulation of endogenous delta opioid receptor signaling can suppress colonic motility without causing constipation. We propose that allosteric modulation of opioid receptor signaling may be a therapeutic strategy to normalize gastrointestinal motility in conditions such as irritable bowel syndrome.

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De Winter, Benedicte Y. "Interplay between inflammation, immune system and neuronal pathways: Effect on gastrointestinal motility." World Journal of Gastroenterology 16, no. 44 (2010): 5523. http://dx.doi.org/10.3748/wjg.v16.i44.5523.

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Martinez, Leopoldo, J. Tovar, and Federica Pederiva. "Enteric Nervous System and Esophageal-Gastrointestinal Motility in Experimental Congenital Diaphragmatic Hernia." European Journal of Pediatric Surgery 24, no. 02 (May 17, 2013): 141–49. http://dx.doi.org/10.1055/s-0033-1345106.

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Schemann, Michael. "Control of Gastrointestinal Motility by the ???Gut Brain??? - The Enteric Nervous System." Journal of Pediatric Gastroenterology and Nutrition 41, Supplement 1 (September 2005): S4—S6. http://dx.doi.org/10.1097/01.scs.0000180285.51365.55.

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OH, Radhika krishna, Mohammed Abdul Aleem, and Geetha Kayla. "Abnormalities of the intestinal pacemaker cells, enteric neurons, and smooth muscle in intestinal atresia." Journal of Laboratory Physicians 11, no. 03 (July 2019): 180–85. http://dx.doi.org/10.4103/jlp.jlp_94_18.

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Abstract BACKGROUND: Small bowel atresia is a congenital disorder that carves a substantial morbidity. Numerous postoperative gastrointestinal motility problems occur. The underlying cause of this motility disorder is still unclear. Interstitial cells of Cajal (ICC) play a major role in gastrointestinal motility. AIMS AND OBJECTIVES: To investigate the morphological changes of enteric nervous system and ICC in small bowel atresia. MATERIAL AND METHODS: Resected small bowel specimen from affected patients (n=15) were divided into three parts (proximal, distal, atretic). Standard histology and immunohistochemistry with anti C-KIT receptor antibody (CD117), calretinin and α-SMA was carried out. The density of myenteric ICCs in the proximal, atretic and distal parts was demonstrated by CD 117 while Calretinin was used for ganglion cells and nerve bundles, α-SMA highlighted muscle hypertrophy. RESULT AND CONCLUSION: The proximal and distal bowel revealed clear changes in the morphology and density of enteric nervous system and interstitial cells of Cajal..

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Tack, J., B. Coulie, A. Wilmer, T. Peeters, and J. Janssens. "Actions of the 5-hydroxytryptamine 1 receptor agonist sumatriptan on interdigestive gastrointestinal motility in man." Gut 42, no. 1 (January 1, 1998): 36–41. http://dx.doi.org/10.1136/gut.42.1.36.

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Background—Pharmacological studies of the enteric nervous system have shown the presence of several subtypes of 5-hydroxytryptamine (5HT) receptor, which might be involved in control of the migrating motor complex.Aims—To study the effect of sumatriptan, an agonist of enteric neuronal 5HT1P receptors, on interdigestive motility in man.Subjects and methods—In 12 healthy subjects, interdigestive motility was recorded manometrically in the upper gastrointestinal tract. In seven subjects blood samples were drawn every 15 minutes for radioimmunoassay of motilin and somatostatin. After two phase 3s of the migrating motor complex, 6 mg of sumatriptan was administered subcutaneously. Recording continued until two more phase 3s had occurred.Results—Sumatriptan induced a premature phase 3 in the jejunum after a median of 10 (8) minutes. The duration of the migrating motor complex cycle was shortened at the expense of phase 2. After sumatriptan, plasma somatostatin concentrations were reduced and gastric phase 3s were suppressed, although median motilin concentrations and the occurrence of plasma motilin peaks were not affected. Phase 3s of the migrating motor complex preceding sumatriptan were associated with motilin peaks, while phase 3s after sumatriptan were not. Furthermore, pretreatment with sumatriptan prevented the induction of a gastric phase 3 by the motilin agonist erythromycin.Conclusions—Administration of the 5HT1P receptor agonist sumatriptan induces a premature intestinal phase 3, suppresses gastric phase 3s, prevents induct- ion of a gastric phase 3 by erythromycin, and reduces plasma somatostatin concentrations.

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Keely, Stephen J., Andreacarola Urso, Alexandr V. Ilyaskin, Christoph Korbmacher, Nigel W. Bunnett, Daniel P. Poole, and Simona E. Carbone. "Contributions of bile acids to gastrointestinal physiology as receptor agonists and modifiers of ion channels." American Journal of Physiology-Gastrointestinal and Liver Physiology 322, no. 2 (February 1, 2022): G201—G222. http://dx.doi.org/10.1152/ajpgi.00125.2021.

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Bile acids (BAs) are known to be important regulators of intestinal motility and epithelial fluid and electrolyte transport. Over the past two decades, significant advances in identifying and characterizing the receptors, transporters, and ion channels targeted by BAs have led to exciting new insights into the molecular mechanisms involved in these processes. Our appreciation of BAs, their receptors, and BA-modulated ion channels as potential targets for the development of new approaches to treat intestinal motility and transport disorders is increasing. In the current review, we aim to summarize recent advances in our knowledge of the different BA receptors and BA-modulated ion channels present in the gastrointestinal system. We discuss how they regulate motility and epithelial transport, their roles in pathogenesis, and their therapeutic potential in a range of gastrointestinal diseases.

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Berry, Dylan T., Joanne Choi, Calla A. Dexheimer, Morgan A. Verhaalen, and Amir Javan-Khoshkholgh. "An Inductively Powered Implantable System to Study the Gastrointestinal Electrophysiology in Freely Behaving Rodents." Bioengineering 9, no. 10 (October 6, 2022): 530. http://dx.doi.org/10.3390/bioengineering9100530.

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Chronic studies in the fasting and fed states of conscious subjects are fundamental for understanding the pathophysiological significance of functional gastrointestinal (GI) disorders and motility dysfunctions. To study the electrophysiology of the GI tract in the long term, the development of gastric implants is essential. This paper presents the development of an implantable system capable of monitoring the bioelectrical activity of the gastric system and modulating the activity in freely behaving rodents. The system consists of a miniature-sized implantable unit (IU), a stationary unit (SU) that communicates with the IU over a 2.4 GHz far-field radio frequency (RF) bidirectional link, and a charging unit (CU) that establishes an inductive 13.56 MHz near-field communication (NFC) with the IU, implementing an adaptive wireless power transfer (WPT). The CU can generate an adjustable power between +20 dBm and +30 dBm, and, in the presence of body movements and stomach motility, can deliver a constant rectified voltage to the IU. The live subject’s exposure to the electromagnetic WPT in the developed system complies with the RF energy absorption restrictions for health and safety concerns. The system can be utilized to investigate the relationship between functional GI disorders and dysrhythmias in the gastric bioelectrical activity and study the potential of electroceutical therapies for motility dysfunctions in clinical settings.

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Frieling, Thomas, Christian Kreysel, Michael Blank, Dorothee Müller, Ilka Melchior, Philipp Euler, Rita Kuhlbusch-Zicklam, Thomas Haarmeier, and Michael Schemann. "Autoimmune encephalitis and gastrointestinal dysmotility: achalasia, gastroparesis, and slow transit constipation." Zeitschrift für Gastroenterologie 58, no. 10 (October 2020): 975–81. http://dx.doi.org/10.1055/a-1233-2190.

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Abstract Background Neurological autoimmune disorders (NAD) are caused by autoimmune inflammation triggered by specific antibody subtypes. NAD may disturb the gut-brain axis at several levels including brain, spinal cord, peripheral, or enteric nervous system. Case report We present a case with antinuclear neuronal Hu (ANNA-1)- and antiglial nuclear (SOX-1) autoimmune antibody-positive limbic encephalitis and significant gastrointestinal dysmotility consisting of achalasia type II, gastroparesis, altered small intestinal interdigestive motility, and severe slow transit constipation. The autoantibodies of the patient’s serum labeled enteric neurons and interstitial cells of Cajal but no other cells in the gut wall. Achalasia was treated successfully by pneumatic cardia dilation and gastrointestinal dysmotility successfully with prucalopride. Conclusion NAD may disturb gastrointestinal motility by altering various levels of the gut-brain axis.

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Rai, Ramesh Roop, and V. G. Mohan Prasad. "Prokinetics in the management of upper gastrointestinal motility disorders: an Indian expert opinion review." International Journal of Advances in Medicine 8, no. 9 (August 21, 2021): 1442. http://dx.doi.org/10.18203/2349-3933.ijam20213253.

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Functional gastrointestinal disorders (FGIDs) are disorders of gut-brain interaction. Nearly 40% of individuals globally suffer from FGIDs and have chronic fluctuating symptoms. Of all GI conditions, 30-45% are referable to intestinal motility disorders. Prokinetics act by different mechanisms and are effective in FGIDs with delayed gastric emptying or postprandial distress. When choosing a prokinetic, safety is the primary concern, particularly with regard to the central nervous system and cardiovascular risk. Here, we review the efficacy and safety of prokinetics in functional GI motility disorders and provide expert opinions for the use of prokinetics to manage upper GI motility disorders in the Indian context.

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Han, Jeong Pil, Jeong Hyeon Lee, Geon Seong Lee, Ok Jae Koo, and Su Cheong Yeom. "Positive Correlation between nNOS and Stress-Activated Bowel Motility Is Confirmed by In Vivo HiBiT System." Cells 10, no. 5 (April 27, 2021): 1028. http://dx.doi.org/10.3390/cells10051028.

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Neuronal nitric oxide synthase (nNOS) has various roles as a neurotransmitter. However, studies to date have produced insufficient data to fully support the correlation between nNOS and bowel motility. This study aimed to investigate the correlation between nNOS expression and gastrointestinal (GI) tract motility using a stress-induced neonatal maternal separation (NMS) mouse model. In this study, we generated a genetically modified mouse with the HiBiT sequence knock-in into the nNOS gene using CRISPR/Cas9 for analyzing accurate nNOS expression. nNOS expression was measured in the stomach, small intestine, large intestine, adrenal gland, and hypothalamus tissues after establishing the NMS model. The NMS model exhibited a significant increase in nNOS expression in large intestine, adrenal gland, and hypothalamus. Moreover, a significant positive correlation was observed between whole gastrointestinal transit time and the expression level of nNOS. We reasoned that NMS induced chronic stress and consequent nNOS activation in the hypothalamic-pituitary-adrenal (HPA) axis, and led to an excessive increase in intestinal motility in the lower GI tract. These results demonstrated that HiBiT is a sensitive and valuable tool for analyzing in vivo gene activation, and nNOS could be a biomarker of the HPA axis-linked lower intestinal tract dysfunction.

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Radocchia, Giulia, Bruna Neroni, Massimiliano Marazzato, Elena Capuzzo, Simone Zuccari, Fabrizio Pantanella, Letizia Zenzeri, et al. "Chronic Intestinal Pseudo-Obstruction: Is There a Connection with Gut Microbiota?" Microorganisms 9, no. 12 (December 10, 2021): 2549. http://dx.doi.org/10.3390/microorganisms9122549.

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Chronic intestinal pseudo-obstruction (CIPO) is a rare clinical syndrome characterized by severe impairment of gastrointestinal (GI) motility, and its symptoms are suggestive of partial or complete intestinal obstruction in the absence of any lesion restricting the intestinal lumen. Diagnosis and therapy of CIPO patients still represent a significant challenge for clinicians, despite their efforts to improve diagnostic workup and treatment strategies for this disease. The purpose of this review is to better understand what is currently known about the relationship between CIPO patients and intestinal microbiota, with a focus on the role of the enteric nervous system (ENS) and the intestinal endocrine system (IES) in intestinal motility, underling the importance of further studies to deeply understand the causes of gut motility dysfunction in these patients.

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Schicho, Rudolf, and Martin Storr. "Alternative Targets Within the Endocannabinoid System for Future Treatment of Gastrointestinal Diseases." Canadian Journal of Gastroenterology 25, no. 7 (2011): 377–83. http://dx.doi.org/10.1155/2011/953975.

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Many beneficial effects of herbal and synthetic cannabinoids on gut motility and inflammation have been demonstrated, suggesting a vast potential for these compounds in the treatment of gastrointestinal disorders. These effects are based on the so-called ‘endocannabinoid system’ (ECS), a cooperating network of molecules that regulate the metabolism of the body’s own and of exogenously administered cannabinoids. The ECS in the gastrointestinal tract quickly responds to homeostatic disturbances by de novo synthesis of its components to maintain homeostasis, thereby offering many potential targets for pharmacological intervention. Of major therapeutic interest are nonpsychoactive cannabinoids or compounds that do not directly target cannabinoid receptors but still possess cannabinoid-like properties. Drugs that inhibit endocannabinoid degradation and raise the level of endocannabinoids are becoming increasingly promising alternative therapeutic tools to manipulate the ECS.

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Ipatov, Andrey A., and Maria G. Ipatova. "Management of functional gastrointestinal disorders in children. Focus on restoring intestinal microenvironment and motility." Meditsinskiy sovet = Medical Council, no. 1 (March 21, 2021): 125–32. http://dx.doi.org/10.21518/2079-701x-2021-1-125-132.

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Functional gastrointestinal disorders in children are one of the most common reasons why parents visit a pediatrician. Functional gastrointestinal disorders include various persistent combinations of chronic or recurrent gastrointestinal symptoms in the absence of any organic pathology in the gastrointestinal tract (structural abnormalities, inflammatory changes, infections, or tumours) and metabolic disturbances. The article presents details on the mechanisms of development, clinical manifestations, diagnostic criteria and approaches to the treatment of functional gastrointestinal disorders. Clinical manifestations of functional gastrointestinal disorders vary depending on age and characteristics of physical and intellectual development. In more than half of children, they are observed in various combinations, less often as one isolated symptom. The drug therapy should consider the main components of pathogenesis and facilitate the solution of the following issues: improvement of digestion; restoration of intestinal microenvironment and motility; reduction of visceral hypersensitivity. Special attention is paid to the management of motor disorders and restoration of intestinal microenvironment using symbiotics. When choosing a supplement, it is advisable to focus on the composition of probiotic strains, which should comply with the WGO global guidelines (Bifidobacterium bifidum, Lactobacillus acidophilus, etc.).Prescription of peripheral δ-, μ- и κ-receptor agonists – trimebutine and pre- and probiotics combinations to children with functional gastrointestinal disorders results in decreased signs of functional disorders of the digestive tract. By acting on the enkephalinergic system, trimebutine regulates the bowel activity, improves motility, and reduces visceral hypersensitivity. Trimebutine is included in the Russian guidelines for the diagnosis and treatment of functional disorders of the digestive tract in children, as well as in the clinical guidelines for the treatment of irritable bowel syndrome, functional dyspepsia, and functional abdominal pain.

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He, Xin, Jing Yang, Ling Qiu, Dan Feng, Feng Ju, Lu Tan, Yu-Zhi Li, et al. "Thiodiketopiperazines Produced by Penicillium crustosum and Their Activities to Promote Gastrointestinal Motility." Molecules 24, no. 2 (January 15, 2019): 299. http://dx.doi.org/10.3390/molecules24020299.

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Three new thiodiketopiperazines (1–3), along with two known analogues (4 and 5), were isolated from the fermentation broth of Penicillium crustosum. Their structures were elucidated through extensive spectroscopic analysis and the absolute configurations of new compounds were determined by Mosher ester analysis and calculated ECD spectra. Compound 4 and 5 have the activity to promote the gastrointestinal motility of zebrafish via acting on the cholinergic nervous system.

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Zhu, Jianping, Lanlan Chang, Jinlu Xie, and Hongbin Ai. "Arginine Vasopressin Injected into the Dorsal Motor Nucleus of the Vagus Inhibits Gastric Motility in Rats." Gastroenterology Research and Practice 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/4618672.

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Background. Until now, the effect of arginine vasopressin (AVP) in the DMV on gastric motility and the possible modulating pathway between the DMV and the gastrointestinal system remain poorly understood.Objectives. We aimed to explore the role of AVP in the DMV in regulating gastric motility and the possible central and peripheral pathways.Material and Methods. Firstly, we microinjected different doses of AVP into the DMV and investigated its effects on gastric motility in rats. Then, the possible central and peripheral pathways that regulate gastric motility were also discussed by microinjectingSR49059(a specific AVP receptor antagonist) into the DMV and intravenous injection of hexamethonium (a specific neuronal nicotinic cholinergic receptor antagonist) before AVP microinjection.Results. Following microinjection of AVP (180 pmol and 18 pmol) into the DMV, the gastric motility (including total amplitude, total duration, and motility index of gastric contraction) was significantly inhibited (P<0.05). Moreover, the inhibitory effect of AVP (180 pmol) on gastric motility could be blocked completely by bothSR49059(320 pmol) and hexamethonium (8 μmol).Conclusions. It is concluded that AVP inhibits the gastric motility by acting on the specific AVP receptor in the DMV, with the potential involvement of the parasympathetic preganglionic cholinergic fibers.

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Romański, KW. "Importance of the enteric nervous system in the control of the migrating motility complex." Physiology International 104, no. 2 (June 2017): 97–129. http://dx.doi.org/10.1556/2060.104.2017.2.4.

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The migrating motility complex (MMC), a cyclical phenomenon, represents rudimentary motility pattern in the gastrointestinal tract. The MMC is observed mostly in the stomach and gut of man and numerous animal species. It contains three or four phases, while its phase III is the most characteristic. The mechanisms controlling the pattern are unclear in part, although the neural control of the MMC seems crucial. The main goal of this article was to discuss the importance of intrinsic innervation of the gastrointestinal tract in MMC initiation, migration, and cessation to emphasize that various MMC-controlling mechanisms act through the enteric nervous system. Two main neural regions, central and peripheral, are able to initiate the MMC. However, central regulation of the MMC may require cooperation with the enteric nervous system. When central mechanisms are not active, the MMC can be initiated peripherally in any region of the small bowel. The enteric nervous system affects the MMC in response to the luminal stimuli which can contribute to the initiation and cessation of the cycle, and it may evoke irregular phasic contractions within the pattern. The hormonal regulators released from the endocrine cells may exert a modulatory effect upon the MMC mostly through the enteric nervous system. Their central action could also be considered. It can be concluded that the enteric nervous system is involved in the great majority of the MMC-controlling mechanisms.

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Montoro-Huguet, Miguel A. "Dietary and Nutritional Support in Gastrointestinal Diseases of the Upper Gastrointestinal Tract (I): Esophagus." Nutrients 14, no. 22 (November 14, 2022): 4819. http://dx.doi.org/10.3390/nu14224819.

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The esophagus is the centerpiece of the digestive system of individuals and plays an essential role in transporting swallowed nutrients to the stomach. Diseases of the esophagus can alter this mechanism either by causing anatomical damage that obstructs the lumen of the organ (e.g., peptic, or eosinophilic stricture) or by generating severe motility disorders that impair the progression of the alimentary bolus (e.g., severe dysphagia of neurological origin or achalasia). In all cases, nutrient assimilation may be compromised. In some cases (e.g., ingestion of corrosive agents), a hypercatabolic state is generated, which increases resting energy expenditure. This manuscript reviews current clinical guidelines on the dietary and nutritional management of esophageal disorders such as severe oropharyngeal dysphagia, achalasia, eosinophilic esophagitis, lesions by caustics, and gastroesophageal reflux disease and its complications (Barrett’s esophagus and adenocarcinoma). The importance of nutritional support in improving outcomes is also highlighted.

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Gonzalez, Zorisadday, Daniel Herlihy, Cong Phan, Jesus Diaz, Kenneth Dominguez, and Richard McCallum. "Alcohol and gastric motility: pathophysiological and therapeutic implications." Journal of Investigative Medicine 68, no. 5 (May 23, 2020): 965–71. http://dx.doi.org/10.1136/jim-2020-001327.

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Alcohol has been associated with alterations in gastric motility. The literature identifies that various factors play a role in alcohol’s effect on gastric emptying including differences in alcohol concentration, osmolarity, caloric content, amino acids as well as different processing techniques (fermentation vs distillation). Additionally, chronic alcohol consumption has been shown to alter the myenteric nitrergic system resulting in impaired gastrointestinal motor function, and it also has an inhibitory effect on the release of several neurotransmitters that play a key role in gastrointestinal motility, including acetylcholine. Whether social or limited intake of alcohol could have a therapeutic role has not been apparent. Serendipitously, we have identified a therapeutic role for alcohol with a meal in the entity of dumping syndrome (DS) where there is postprandial rapid emptying of voluminous and hyperosmolar gastric contents into the small bowel. In the clinical setting of DS attributed to impaired vagal nerve function, there was normalization of gastric emptying and resolution of accompanying symptoms when drinking a glass of wine before and during meals. We propose that alcohol’s anticholinergic effect was augmented in the setting of vagal nerve denervation resulting in slowing of gastric emptying and in alleviation of symptoms of early DS. This review article provides an in-depth analysis of the published literature on alcohol and gastric motility focusing on the accumulated knowledge that may have clinical application and relevance.

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Marathe, Chinmay S., Christopher K. Rayner, Karen L. Jones, and Michael Horowitz. "Effects of GLP-1 and Incretin-Based Therapies on Gastrointestinal Motor Function." Experimental Diabetes Research 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/279530.

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Glucagon-like peptide 1 (GLP-1) is a hormone secreted predominantly by the distal small intestine and colon and released in response to enteral nutrient exposure. GLP-1-based therapies are now used widely in the management of type 2 diabetes and have the potential to be effective antiobesity agents. Although widely known as an incretin hormone, there is a growing body of evidence that GLP-1 also acts as an enterogastrone, with profound effects on the gastrointestinal motor system. Moreover, the effects of GLP-1 on gastrointestinal motility appear to be pivotal to its effect of reducing postprandial glycaemic excursions and may, potentially, represent the dominant mechanism. This review summarizes current knowledge of the enterogastrone properties of GLP-1, focusing on its effects on gut motility at physiological and pharmacological concentrations, and the motor actions of incretin-based therapies. While of potential importance, the inhibitory action of GLP-1 on gastric acid secretion is beyond the scope of this paper.

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Fu, Rong-Guo, Heng Ge, Gang-Lian Yao, Li Wang, Shu-Ting Ren, Li-Qun Ma, Bao-Song Gui, Zhao Chen, Dan Zhu, and Rong-Liang Xue. "Uremic anorexia and gastrointestinal motility dysfunction correlate with the changes of ghrelin system in hypothalamus." Nephrology 18, no. 2 (January 20, 2013): 111–16. http://dx.doi.org/10.1111/nep.12015.

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Kruse-Andersen, S., J. Kolberg, and E. Jakobsen. "Neural Network for Automatic Analysis of Motility Data." Methods of Information in Medicine 33, no. 01 (1994): 157–60. http://dx.doi.org/10.1055/s-0038-1634978.

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Abstract:Continuous recording of intraluminal pressures for extended periods of time is currently regarded as a valuable method for detection of esophageal motor abnormalities. A subsequent automatic analysis of the resulting motility data relies on strict mathematical criteria for recognition of pressure events. Due to great variation in events, this method often fails to detect biologically relevant pressure variations. We have tried to develop a new concept for recognition of pressure events based on a neural network. Pressures were recorded for over 23 hours in 29 normal volunteers by means of a portable data recording system. A number of pressure events and non-events were selected from 9 recordings and used for training the network. The performance of the trained network was then verified on recordings from the remaining 20 volunteers. The accuracy and sensitivity of the two systems were comparable. However, the neural network recognized pressure peaks clearly generated by muscular activity that had escaped detection by the conventional program. In conclusion, we believe that neu-rocomputing has potential advantages for automatic analysis of gastrointestinal motility data.

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Tougas, Gervais. "The Autonomic Nervous System in Functional Bowel Disorders." Canadian Journal of Gastroenterology 13, suppl a (1999): 15A—17A. http://dx.doi.org/10.1155/1999/707105.

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Communications along the brain-gut axis involve neural pathways as well as immune and endocrine mechanisms. The two branches of the autonomic nervous system are integrated anatomically and functionally with visceral sensory pathways, and are responsible for the homeostatic regulation of gut function. The autonomic nervous system is also a major mediator of the visceral response to central influences such as psychological stress. As defined, functional disorders comprise a constellation of symptoms, some of which suggest the presence of altered perception, while other symptoms point to disordered gastrointestinal function as the cause of the symptoms. A growing number of reports have demonstrated disordered autonomic function in subgroups of functional bowel patients. While a number of different methods were used to assess autonomic function, the reports point to a generally decreased vagal (parasympathetic) outflow or increased sympathetic activity in conditions usually associated with slow or decreased gastrointestinal motility, while other studies found either an increased cholinergic activity or a decreased sympathetic activity in patients with symptoms compatible with an increased motor activity. Under certain conditions, altered autonomic balance (including low vagal tone and increased sympathetic activity) may alter visceral perception. Autonomic dysfunction may also represent the physiological pathway accounting for many of the extraintestinal symptoms seen in irritable bowel syndrome patients and some of the frequent gastrointestinal complaints reported by patients with disorders such as chronic fatigue and fibromyalgia.

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Iwasaki, Mari, Yasutada Akiba, and Jonathan D. Kaunitz. "Recent advances in vasoactive intestinal peptide physiology and pathophysiology: focus on the gastrointestinal system." F1000Research 8 (September 12, 2019): 1629. http://dx.doi.org/10.12688/f1000research.18039.1.

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Vasoactive intestinal peptide (VIP), a gut peptide hormone originally reported as a vasodilator in 1970, has multiple physiological and pathological effects on development, growth, and the control of neuronal, epithelial, and endocrine cell functions that in turn regulate ion secretion, nutrient absorption, gut motility, glycemic control, carcinogenesis, immune responses, and circadian rhythms. Genetic ablation of this peptide and its receptors in mice also provides new insights into the contribution of VIP towards physiological signaling and the pathogenesis of related diseases. Here, we discuss the impact of VIP on gastrointestinal function and diseases based on recent findings, also providing insight into its possible therapeutic application to diabetes, autoimmune diseases and cancer.

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Schonkeren, Simone L., Meike S. Thijssen, Nathalie Vaes, Werend Boesmans, and Veerle Melotte. "The Emerging Role of Nerves and Glia in Colorectal Cancer." Cancers 13, no. 1 (January 5, 2021): 152. http://dx.doi.org/10.3390/cancers13010152.

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The role of the nervous system as a contributor in the tumor microenvironment has been recognized in different cancer types, including colorectal cancer (CRC). The gastrointestinal tract is a highly innervated organ system, which is not only innervated by the autonomic nervous system, but also contains an extensive nervous system of its own; the enteric nervous system (ENS). The ENS is important for gut function and homeostasis by regulating processes such as fluid absorption, blood flow, and gut motility. Dysfunction of the ENS has been linked with multiple gastrointestinal diseases, such as Hirschsprung disease and inflammatory bowel disease, and even with neurodegenerative disorders. How the extrinsic and intrinsic innervation of the gut contributes to CRC is not fully understood, although a mutual relationship between cancer cells and nerves has been described. Nerves enhance cancer progression through the secretion of neurotransmitters and neuropeptides, and cancer cells are capable of stimulating nerve growth. This review summarizes and discusses the nervous system innervation of the gastrointestinal tract and how it can influence carcinogenesis, and vice versa. Lastly, the therapeutic potential of these novel insights is discussed.

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Boillat, Carol S., Frédéric P. Gaschen, Lorrie Gaschen, Rhett W. Stout, and Giselle L. Hosgood. "Variability associated with repeated measurements of gastrointestinal tract motility in dogs obtained by use of a wireless motility capsule system and scintigraphy." American Journal of Veterinary Research 71, no. 8 (August 2010): 903–8. http://dx.doi.org/10.2460/ajvr.71.8.903.

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Jørgensen, D., J. L. Poulsen, A. E. Olesen, C. Brock, T. H. Sandberg, K. Krogh, and A. M. Drewes. "The impact of opioid treatment on regional gastrointestinal transit." Scandinavian Journal of Pain 12, no. 1 (July 1, 2016): 126. http://dx.doi.org/10.1016/j.sjpain.2016.05.029.

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AbstractAimsTo employ a human experimental model of opioid-induced bowel dysfunction (OIBD) in healthy volunteers, and evaluate the impact of opioid treatment compared to placebo on gastrointestinal (GI) symptoms and motility, assessed by questionnaires and regional GI transit times.MethodsTwenty-five healthy males were randomly assigned to oxycodone or placebo for five days in a double-blind, crossover design. Adverse GI effects were measured with bowel function index, gastrointestinal symptom rating scale, patient assessment of constipation symptoms questionnaire, and bristol stool form scale. Regional GI transit times were determined using the 3D-Transit system and segmental colonic transit times were determined using a custom Matlab® graphical user interface.ResultsGI symptom scores increased significantly across all applied questionnaires during opioid treatment. Oxycodone increased median total GI transit time from 22.2 to 43.9 h (P< 0.01), segmental transit times in the cecum and ascending colon from 5.7 to 9.9 h (P<0.05), rectosigmoid transit time from 2.7 to 9.0 h (P<0.05), and colorectal transit time from 18.6 to 38.6 h (P<0.01). No association between questionnaire scores and segmental transit times were detected.ConclusionsSelf-assessed adverse GI effects and increased GI transit times in different segments were induced during oxycodone treatment. This detailed information about segmental changes in motility has great potential for future interventional head-to-head trials of different laxative regimes for prevention and treatment of OIBD.

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Spak, Emma, Peter Hallersund, Anders Edebo, Anna Casselbrant, and Lars Fändriks. "The human duodenal mucosa harbors all components for a local renin angiotensin system." Clinical Science 133, no. 8 (April 2019): 971–82. http://dx.doi.org/10.1042/cs20180877.

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Abstract The renin-angiotensin system (RAS) is present in the gastrointestinal (GI) tract but remains to be fully characterized, particularly in man. The duodenum plays a role in both the upper and lower GI regulation, as well as in distant organs. The present study investigates the presence and functional potential of RAS in the human duodenal mucosa of healthy individuals. Endoscopically acquired mucosal biopsies from healthy volunteers were examined using western blot, immunohistochemistry, and ELISA. Functionality was examined by using Ussing chambers and recording duodenal transmucosal potential difference (PD) and motility in vivo. Angiotensinogen, Angiotensin II (AngII) and its receptors (AT1R, AT2R) as well as to the RAS associated enzymes renin, ACE, and neprylisin were detected in all samples of duodenal mucosa. Migrating motility complex induced elevations of transmucosal PD were significantly larger after per-oral administration of the AT1R receptor antagonist candesartan. Fasting duodenal motility per se was not influenced by candesartan. The epithelial current produced by duodenal mucosae mounted in Ussing chambers increased significantly after addition of AngII to specimens where the AT1R was blocked using losartan. The epithelial current also increased after addition of the AT2R-selective agonist C21. Immunostaining and pharmacological data demonstrate the presence of a local RAS in the human duodenal mucosa with capacity to influence epithelial ion transport by way of particulary the AT2R.

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Jones, Michael A., Kerrie L. Marston, Claire A. Woodall, Duncan J. Maskell, Dennis Linton, Andrey V. Karlyshev, Nick Dorrell, Brendan W. Wren, and Paul A. Barrow. "Adaptation of Campylobacter jejuni NCTC11168 to High-Level Colonization of the Avian Gastrointestinal Tract." Infection and Immunity 72, no. 7 (July 2004): 3769–76. http://dx.doi.org/10.1128/iai.72.7.3769-3776.2004.

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ABSTRACT The genome sequence of the human pathogen Campylobacter jejuni NCTC11168 has been determined recently, but studies on colonization and persistence in chickens have been limited due to reports that this strain is a poor colonizer. Experimental colonization and persistence studies were carried out with C. jejuni NCTC11168 by using 2-week-old Light Sussex chickens possessing an acquired natural gut flora. After inoculation, NCTC11168 initially colonized the intestine poorly. However, after 5 weeks we observed adaptation to high-level colonization, which was maintained after in vitro passage. The adapted strain exhibited greatly increased motility. A second strain, C. jejuni 11168H, which had been selected under in vitro conditions for increased motility (A. V. Karlyshev, D. Linton, N. A. Gregson, and B. W. Wren, Microbiology 148:473-480, 2002), also showed high-level intestinal colonization. The levels of colonization were equivalent to those of six other strains, assessed under the same conditions. There were four mutations in C. jejuni 11168H that reduced colonization; maf5, flaA (motility and flagellation), and kpsM (capsule deficiency) eliminated colonization, whereas pglH (general glycosylation system deficient) reduced but did not eliminate colonization. This study showed that there was colonization of the avian intestinal tract by a Campylobacter strain having a known genome sequence, and it provides a model for colonization and persistence studies with specific mutations.

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Jiang, Yanyan, Tanja Babic, and R. Alberto Travagli. "Sex differences in GABAergic neurotransmission to rat DMV neurons." American Journal of Physiology-Gastrointestinal and Liver Physiology 317, no. 4 (October 1, 2019): G476—G483. http://dx.doi.org/10.1152/ajpgi.00112.2019.

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Functional gastrointestinal disorders, including delayed gastric emptying and decreased gastric motility, are more prevalent in women, suggesting a potential role for circulating gonadal hormones, including estrogen. Gastric motility is tuned by the vagal inputs arising from the dorsal motor nucleus of the vagus (DMV), which is itself controlled by tonic GABAergic inputs. Estrogen increases GABA functions in various central nervous system areas; however, the effect of the estrus cycle in modulating GABAergic inputs onto DMV neurons, hence vagal control of gastric motility, has not been investigated. The aim of the present study was to test the hypothesis that GABAergic tone to DMV neurons, hence the vagal output to the stomach, varies according to sex and the estrus cycle. Experiments were performed on age-matched Sprague-Dawley male and virgin female rats; females were subdivided according to the high-estrogen (HE) or low-estrogen (LE) period of their cycle. Whole-cell patch-clamp recordings were made from gastric-projecting DMV neurons, and the response to perfusion with the GABAA receptor antagonist bicuculline was examined. The response of corpus and antrum tone and motility to bicuculline microinjected in the dorsal vagal complex, recorded via strain gauges sewn to the anterior gastric surface, was also assessed. Bicuculline increased the firing rate of DMV neurons, as well as gastric tone and motility, to a larger extent in HE compared with LE or male rats, suggesting a higher GABAergic tone in HE female rats. Taken together, the data support the hypothesis that GABAergic tone to DMV neurons varies according to sex and estrus cycle. NEW & NOTEWORTHY GABAergic neurotransmission to the dorsal motor nucleus of the vagus (DMV) plays a pivotal role in the modulation of gastric tone and motility. Gastric motility is reduced in women and may contribute to the higher incidence of functional gastrointestinal disorders. In the present study, we report that GABAergic tone to rat DMV neurons, hence vagal output to the stomach, varies according to sex and estrus cycle, and the GABAergic tone is increased during the high-estrogen period of the estrus cycle.

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Ruparelia, Darshan, Ganpat Devpura, Rakesh Thakuriya, and Bindu Rani. "Study of Autonomic Neuropathy in Cardiovascular System in Chronic Renal Failure Patients on Maintenance Hemodialysis." East African Scholars Journal of Medical Sciences 5, no. 2 (February 15, 2022): 35–38. http://dx.doi.org/10.36349/easms.2022.v05i02.002.

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Autonomic nervous system abnormalities are major causes of morbidity and mortality in patients with chronic renal failure (CRF) on hemodialysis and are generally considered a part of polyneuropathy. Postural hypotension, impotency, gastrointestinal disturbance, gastrointestinal motility, and sweating abnormalities are common symptoms. The most frequent complication in patients with CRF on hemodialysis is intradialytic hypotension, and it has been suggested that intradialytic hypotension is mostly related to autonomic neuropathy. The pathogenesis of autonomic neuropathy is unclear, but a reduced response to norepinephrine by the end organ and the toxic effect of metabolic toxins are considered to be some of the causes. Five cardiovascular reflex tests are generally used to determine autonomic neuropathy: the heart rate reaction to the Valsalva Maneuver, the heart rate variability during deep breathing, the heart rate response to standing up, the blood pressure response to standing up, and the blood pressure response to hand grip exercise.

Статті в журналах з теми "Gastrointestinal system Motility"

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