scholarly journals Gastrointestinal Motility, Mucosal Mast Cell, and Intestinal Histology in Rats: Effect of Prednisone

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Maysa Bruno de Lima ◽  
Loyane Almeida Gama ◽  
Andrieli Taise Hauschildt ◽  
Denize Jussara Rupolo Dall’Agnol ◽  
Luciana Aparecida Corá ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Mast Cells ◽  
Gastrointestinal Motility ◽  
Experimental Studies ◽  
Control Group ◽  
Mucosal Mast Cell ◽  
Intestinal Histology ◽  
Adult Rats ◽  
Small Intestinal Transit ◽  
Mucosal Mast Cells

Our aim was to verify the effects of prednisone related to gastrointestinal motility, intestinal histology, and mucosal mast cells in rats. Two-month-old male Wistar rats were randomly assigned to control group (vehicle) animals receiving saline 0.9% (n=7) or treated orally with 0.625 mg/kg/day of prednisone (n=7) or 2.5 mg/kg/day of prednisone (n=7) during 15 days. Mast cells and other histologic analyses were performed in order to correlate to gastric emptying, cecum arrival, and small intestine transit evaluated by Alternating Current Biosusceptometry. Results showed that prednisone in adult rats increased the frequency of gastric contractions, hastened gastric emptying, slowed small intestinal transit, and reduced mucosal mast cells. Histologically, the treatment with both doses of prednisone decreased villus height, whereas longitudinal and circular muscles and crypt depth were not affected. These findings indicate an impairment of intestinal absorption which may be linked to several GI dysfunctions and symptoms. The relationship between gastrointestinal motor disorders and cellular immunity needs to be clarified in experimental studies since prednisone is one of the most prescribed glucocorticoids worldwide.

Mucosal mast cells are involved in CCK disruption of MMC in the rat intestine

1998 ◽  
Vol 275 (1) ◽  
pp. G63-G67 ◽  
Author(s):  
Carme Juanola ◽  
Magda Giralt ◽  
Marcel Jiménez ◽  
Marisabel Mourelle ◽  
Patri Vergara
Keyword(s):  
Mast Cell ◽  
Small Intestine ◽  
Mast Cells ◽  
Control Group ◽  
Rat Intestine ◽  
Pancreatic Acini ◽  
Mast Cell Stabilizer ◽  
Mucosal Mast Cells ◽  
Stimulation Of ◽  
Cck Release

Our aim was to determine if mucosal mast cells could be activated by endogenous CCK and, as a consequence, mediate CCK actions in the small intestine. Rats were prepared for electromyography to record electrical activity in the small intestine. In another group of animals, the duodenum was perfused to measure rat mast cell protease II (RMCP II) as indicative of mast cell degranulation. Endogenous CCK release was induced by administration of soybean trypsin inhibitor (SBTI) in conscious rats or by intraduodenal perfusion of ovalbumin hydrolysate (OVH) in anesthetized rats. CCK concentration was measured by bioassay on pancreatic acini. SBTI in control rats disrupted migrating motor complexes (MMC) for >40 min. In rats treated with the mast cell stabilizer ketotifen, SBTI did not induce any change in the MMC pattern. RMCP II concentration in the duodenal perfusate significantly increased after OVH. Perfusate from ketotifen-treated animals did not show any significant increase in RMCP II values during OVH perfusion, although CCK plasma concentration was not different from the control group. Furthermore, infusion of the CCK-B receptor antagonist L-365,260 significantly blocked the increase of RMCP II concentration after OVH. Our results indicate that mucosal mast cells are degranulated by endogenous CCK release through stimulation of CCK-B receptors. Therefore mucosal mast cells participate in CCK intestinal actions.

Mucosal mast cells and developmental changes in gastric absorption

1995 ◽  
Vol 268 (1) ◽  
pp. G121-G127 ◽  
Author(s):  
A. G. Catto-Smith ◽  
J. L. Ripper
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Short Circuit ◽  
Mast Cell Degranulation ◽  
Mucosal Mast Cell ◽  
Sprague Dawley ◽  
Mucosal Permeability ◽  
Mucosal Mast Cells ◽  
Gastric Mucosal Mast Cell

We aimed to establish whether gastric mucosal mast cells undergo degranulation during normal postnatal development and to correlate this with gastric electrical parameters, paracellular permeability, and macromolecular absorption. Sprague-Dawley rats were studied between 10 and 30 days after birth. Gastric mucosal mast cell degranulation occurred and was maximal on days 15 and 17, measured by histology and gastric and serum levels of rat mast cell protease II. Short-circuit current, transepithelial conductance, and permeability of voltage-clamped glandular stomach were elevated in younger animals, falling with age except for a transient but significant increase in conductance and permeability at 17 days, closely correlated with maximal mast cell degranulation. Macromolecular uptake was significantly increased in animals aged 10-15 days. Concanavalin A and antigen-induced mast cell degranulation increased conductance and permeability in vitro in younger animals. We conclude that 1) gastric mucosal mast cells degranulate during development, 2) the neonatal stomach has increased permeability and uptake of macromolecules, and 3) gastric mucosal mast cell degranulation during development may affect mucosal permeability.

Prokinetic effects of mirtazapine on gastrointestinal transit

2014 ◽  
Vol 306 (9) ◽  
pp. G796-G801 ◽  
Author(s):  
Jieyun Yin ◽  
Jun Song ◽  
Yong Lei ◽  
Xiaohong Xu ◽  
Jiande D. Z. Chen
Keyword(s):  
Gastric Emptying ◽  
Gastrointestinal Motility ◽  
Gastrointestinal Transit ◽  
Gastrointestinal Diseases ◽  
Colonic Transit ◽  
Small Intestinal Transit ◽  
Gastric Tone ◽  
Healthy Dogs ◽  
Small Intestinal ◽  
Rectal Distention

Mirtazapine is a noradrenergic and specific serotonergic antidepressant. The aim of this study was to investigate the effects of mirtazapine on gastrointestinal motility in dogs, including solid gastric emptying, antral and small intestinal contractions, and small intestinal and colonic transit. Six dogs were implanted with two cannulas located at the duodenum and the ascending colon; another six dogs were implanted with gastric cannula 6 cm proximal to the pylorus. Mirtazapine 45 mg was administered orally 90 min before the study. We found that 1) Mirtazapine accelerated gastric emptying during the entire 3 h in normal dogs ( P < 0.04) and accelerated delayed gastric emptying induced by rectal distention ( P < 0.04). 2) Mirtazapine restored impaired gastric tone and accommodation induced by rectal distention ( P < 0.05). 3) No significant changes were noted in small intestinal contractions or transit with mirtazapine ( P > 0.1). 4) Mirtazapine accelerated colonic transit at 2 and 4 h but not 6 h. The geometric center was increased from 1.9 ± 0.6 to 3.0 ± 0.5 and 3.9 ± 0.5 to 4.7 ± 0.1 at 2 and 4 h respectively ( P = 0.04 vs. corresponding control). In conclusion, mirtazapine improves gastric emptying in healthy dogs and normalizes rectal distention-induced delay in gastric emptying and accelerates colon but not small intestinal transit in healthy dogs. Clinical studies are warranted to assess the effects of mirtazapine on gastrointestinal motility and sensory functions in patients with functional gastrointestinal diseases.

scholarly journals Mucosal Mast Cells in Irritable Bowel Syndrome and Inflammatory Bowel Disease

2005 ◽  
Vol 48 (3-4) ◽  
pp. 163-164 ◽  
Author(s):  
Bilge Tunc ◽  
Levent Filik ◽  
Engin Altıntas ◽  
Nesrin Turhan ◽  
Aysel Ulker ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Mast Cell ◽  
Irritable Bowel Syndrome ◽  
Mast Cells ◽  
Bowel Disease ◽  
Mucosal Mast Cell ◽  
Cell Counts ◽  
Mucosal Mast Cells ◽  
Inflammatory Bowel ◽  
Irritable Bowel

Even though exciting progresses have been until now, further studies are necessary to clearly understand the significance of MMC. Mast cells are thought to participate in the pathogenesis of inflammatory bowel disease and irritable bowel syndrome. However, their role in the pathogenesis remains unsettled. The specific aims of this study were to (1) examine mucosal mast cell counts in the cecum in patient with IBS, and IBD (2) compare MMC between the disease groups. We showed increased MMC count in IBS.

scholarly journals Does Hypothyroidism Affect Gastrointestinal Motility?

2009 ◽  
Vol 2009 ◽  
pp. 1-7 ◽  
Author(s):  
Olga Yaylali ◽  
Suna Kirac ◽  
Mustafa Yilmaz ◽  
Fulya Akin ◽  
Dogangun Yuksel ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Gastrointestinal Motility ◽  
Primary Hypothyroidism ◽  
Dynamic Imaging ◽  
Control Group ◽  
Esophageal Transit ◽  
Gastric Emptying Scintigraphy ◽  
Esophageal Scintigraphy ◽  
Gastric Emptying Time ◽  
Healthy Females

Background. Gastrointestinal motility and serum thyroid hormone levels are closely related. Our aim was to analyze whether there is a disorder in esophagogastric motor functions as a result of hypothyroidism.Materials and Methods. The study group included 30 females (mean age ± SE 45.17 ± 2.07 years) with primary hypothyroidism and 10 healthy females (mean age ± SE 39.40 ± 3.95 years). All cases underwent esophagogastric endoscopy and scintigraphy. For esophageal scintigraphy, dynamic imaging of esophagus motility protocol, and for gastric emptying scintigraphy, anterior static gastric images were acquired.Results. The mean esophageal transit time (52.56 ± 4.07 sec for patients; 24.30 ± 5.88 sec for controls;P=.02) and gastric emptying time (49.06 ± 4.29 min for the hypothyroid group; 30.4 ± 4.74 min for the control group;P=.01) were markedly increased in cases of hypothyroidism.Conclusion. Hypothyroidism prominently reduces esophageal and gastric motor activity and can cause gastrointestinal dysfunction.

scholarly journals Role of mucosal mast cells in early vascular permeability changes of intestinal DTH reaction in the rat

1998 ◽  
Vol 274 (5) ◽  
pp. G832-G839 ◽  
Author(s):  
Aletta D. Kraneveld ◽  
Thea Muis ◽  
Andries S. Koster ◽  
Frans P. Nijkamp
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Activation ◽  
Vascular Leakage ◽  
Mast Cell Activation ◽  
Mucosal Mast Cell ◽  
Mucosal Mast Cells

Previously, it was shown that depletion and stabilization of the mucosal mast cell around the time of challenge were very effective in reducing delayed-type hypersensitivity (DTH) reactions in the small intestine of the rat. The role of mucosal mast cells in the early component of intestinal DTH reaction was further investigated in this study. In vivo small intestinal vascular leakage and serum levels of rat mast cell protease II (RMCP II) were determined within 1 h after intragastric challenge of rats that had been sensitized with dinitrobenzene 5 days before. A separate group of rats was used to study vasopermeability in isolated vascularly perfused small intestine after in vitro challenge. To investigate the effects of mast cell stabilization on the early events of the DTH reaction, doxantrazole was used. The influence of sensory nerves was studied by means of neonatal capsaicin-induced depletion of sensory neuropeptides. Within 1 h after challenge, a significant increase in vascular permeability was found in vivo as well as in vitro. This was associated with a DTH-specific increase in RMCP II in the serum, indicating mucosal mast cell activation. In addition, doxantrazole treatment and caspaicin pretreatment resulted in a significant inhibition of the DTH-induced vascular leakage and an increase in serum RMCP II. These findings are consistent with an important role for mucosal mast cells in early vascular leakage changes of intestinal DTH reactions. In addition, sensory nervous control of mucosal mast cell activation early after challenge is demonstrated.

Lipid-rich enteral nutrition regulates mucosal mast cell activation via the vagal anti-inflammatory reflex

2013 ◽  
Vol 305 (5) ◽  
pp. G383-G391 ◽  
Author(s):  
Jacco J. de Haan ◽  
M'hamed Hadfoune ◽  
Tim Lubbers ◽  
Caroline Hodin ◽  
Kaatje Lenaerts ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Activation ◽  
Mast Cell Activation ◽  
Mucosal Mast Cell ◽  
Mucosal Mast Cells ◽  
Vagal Reflex ◽  
Anti Inflammatory ◽  
Mouse Mast Cell ◽  
Stimulation Of

Nutritional stimulation of the cholecystokinin-1 receptor (CCK-1R) and nicotinic acetylcholine receptor (nAChR)-mediated vagal reflex was shown to reduce inflammation and preserve intestinal integrity. Mast cells are important early effectors of the innate immune response; therefore modulation of mucosal mast cells is a potential therapeutic target to control the acute inflammatory response in the intestine. The present study investigates intestinal mast cell responsiveness upon nutritional activation of the vagal anti-inflammatory reflex during acute inflammation. Mucosal mast cell degranulation was induced in C57/Bl6 mice by administration of Salmonella enterica LPS. Lipid-rich enteral feeding prior to LPS significantly decreased circulatory levels of mouse mast cell protease at 30 min post-LPS compared with isocaloric low-lipid nutrition or fasting. CCK-1R blockage reversed the inhibitory effects of lipid-rich feeding, whereas stimulation of the peripheral CCK-1R mimicked nutritional mast cell inhibition. The effects of lipid-rich nutrition were negated by nAChR blockers chlorisondamine and α-bungarotoxin and vagal intestinal denervation. Accordingly, release of β-hexosaminidase by MC/9 mast cells following LPS or IgE-ovalbumin complexes was dose dependently inhibited by acetylcholine and nicotine. Application of GSK1345038A, a specific agonist of the nAChR α7, in bone marrow-derived mast cells from nAChR β2−/− and wild types indicated that cholinergic inhibition of mast cells is mediated by the nAChR α7 and is independent of the nAChR β2. Together, the present study reveals mucosal mast cells as a previously unknown target of the nutritional anti-inflammatory vagal reflex.

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