18 results on '"Rectum drug effects"'
Search Results
2. Levels of rectal mucosal polyamines and prostaglandin E2 predict ability of DFMO and sulindac to prevent colorectal adenoma.
- Author
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Thompson PA, Wertheim BC, Zell JA, Chen WP, McLaren CE, LaFleur BJ, Meyskens FL, and Gerner EW
- Subjects
- Adenoma metabolism, Adenoma pathology, Adenoma surgery, Aged, Biomarkers, Pharmacological metabolism, Biopsy, Colonoscopy, Colorectal Neoplasms metabolism, Colorectal Neoplasms pathology, Colorectal Neoplasms surgery, Double-Blind Method, Drug Therapy, Combination, Female, Humans, Intestinal Mucosa drug effects, Intestinal Mucosa metabolism, Likelihood Functions, Logistic Models, Male, Middle Aged, Neoplasms, Second Primary metabolism, Neoplasms, Second Primary pathology, Putrescine metabolism, Rectum metabolism, Rectum pathology, Rectum surgery, Spermidine metabolism, Spermine metabolism, Time Factors, Treatment Outcome, Adenoma prevention & control, Anticarcinogenic Agents therapeutic use, Colorectal Neoplasms prevention & control, Dinoprostone metabolism, Eflornithine therapeutic use, Enzyme Inhibitors therapeutic use, Neoplasms, Second Primary prevention & control, Polyamines metabolism, Rectum drug effects, Sulindac therapeutic use
- Abstract
Background & Aims: Combination of polyamine and prostaglandin E2 (PGE2)-synthesis inhibitors reduced the risk of colorectal adenoma (CRA) by 70% in patients who received polypectomies. We studied effects of the combination of difluoromethylornithine (DFMO) and sulindac on biomarkers and investigated factors that modify their efficacy., Methods: We analyzed rectal mucosal levels of polyamines (spermidine, spermine, and putrescine) and PGE2, treatment regimens, and risk of CRA in 267 participants of a phase IIb/III chemoprevention trial of DFMO/sulindac., Results: In the group that received DFMO/sulindac, spermidine-to-spermine ratio (Spd:Spm) in rectal mucosa decreased between baseline and 12- and 36-month follow-up examinations (0.30, 0.23, and 0.24, respectively; P < .001 for both comparisons to baseline). Putrescine levels decreased between baseline and 12 months (0.46 vs 0.15 nmol/mg protein; P < .001) but rebounded between 12 and 36 months (0.15 vs 0.36 nmol/mg protein; P = .001). PGE2 levels did not change, although aspirin use was significantly associated with lower baseline levels of PGE2. No significant associations were observed between changes in biomarker levels and efficacy. However, drug efficacy was greatest in subjects with low Spd:Spm and high PGE2 at baseline; none of these subjects, versus 39% of those given placebo, developed CRA (P < .001). Efficacy was lowest in subjects with high Spd:Spm and low PGE2 at baseline; 28% developed CRA, compared with 36% of patients given placebo (P = .563)., Conclusions: A combination of DFMO and sulindac significantly suppressed production of rectal mucosal polyamines but not PGE2. No relationship was found between changes in biomarker levels and response. However, baseline biomarker levels modified the effect of DFMO/sulindac for CRA prevention., (Copyright © 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.)
- Published
- 2010
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3. Rectal instillation of butyrate provides a novel clinically relevant model of noninflammatory colonic hypersensitivity in rats.
- Author
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Bourdu S, Dapoigny M, Chapuy E, Artigue F, Vasson MP, Dechelotte P, Bommelaer G, Eschalier A, and Ardid D
- Subjects
- Animals, Butyrates administration & dosage, Colonic Diseases physiopathology, Dose-Response Relationship, Drug, Enema veterinary, Female, Humans, Hyperalgesia etiology, Hypersensitivity, Male, Pain etiology, Rats, Rats, Sprague-Dawley, Rectum drug effects, Butyrates adverse effects, Colonic Diseases immunology, Disease Models, Animal, Irritable Bowel Syndrome physiopathology, Receptors, Calcitonin Gene-Related Peptide physiology
- Abstract
Background & Aims: The treatment of irritable bowel syndrome (IBS), characterized by abdominal pain and bloating, is empirical and often poorly efficient. Research lacks suitable models for studying the pathophysiologic mechanisms of the colonic hypersensitivity and new pharmacologic targets. The present study aimed to develop a novel model of colonic hypersensitivity possessing several of the characteristics encountered in patients with IBS., Methods: Rats received enemas of a butyrate solution (8-1000 mmol/L) twice daily for 3 days. A time course was determined for colonic hypersensitivity (colorectal distention test) and referred cutaneous lumbar hyperalgesia (von Frey hairs). Macroscopic and histologic analyses were performed on colonic mucosa. The efficacy of morphine, U50488H (a kappa opioid agonist), and trimebutine on the 2 pain parameters was determined. Finally, the involvement of peptidergic C-fibers was evaluated using capsaicin-pretreated animals and treatments with calcitonin gene-related peptide (CGRP) and neurokinin 1 receptor antagonists., Results: Butyrate enemas induced a sustained, concentration-dependent colonic hypersensitivity and, to a lesser extent, a referred cutaneous mechanical hyperalgesia, particularly in female rats, but no macroscopic and histologic modifications of the colonic mucosa, as observed in patients with IBS. Both pain parameters were sensitive to morphine, U50488H, trimebutine, neonatal capsaicin treatment, and the CGRP receptor antagonist but not to the neurokinin 1 receptor antagonist., Conclusions: These results present our noninflammatory model of chronic colonic hypersensitivity as a useful novel tool for studying IBS. The CGRP receptor antagonist-induced reduction of colonic hypersensitivity suggests that CGRP receptors may provide a promising target for treatment of IBS.
- Published
- 2005
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4. Immunohistochemical demonstration of the NK(1) tachykinin receptor on muscle and epithelia in guinea pig intestine.
- Author
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Southwell BR and Furness JB
- Subjects
- Animals, Carbocyanines metabolism, Carbocyanines pharmacology, Colon cytology, Colon innervation, Endocytosis drug effects, Epithelial Cells chemistry, Epithelial Cells metabolism, Female, Fluorescent Dyes metabolism, Fluorescent Dyes pharmacology, Guinea Pigs, Immunohistochemistry, Intestinal Mucosa cytology, Intestinal Mucosa innervation, Intestine, Small cytology, Intestine, Small innervation, Male, Muscle, Smooth innervation, Nerve Fibers chemistry, Neurokinin-1 Receptor Antagonists, Piperidines pharmacology, Receptors, Neurokinin-1 metabolism, Receptors, Neurokinin-2 analysis, Receptors, Neurokinin-2 metabolism, Receptors, Neurokinin-3 analysis, Receptors, Neurokinin-3 metabolism, Rectum drug effects, Rectum physiology, Substance P pharmacology, Intestinal Mucosa chemistry, Muscle, Smooth chemistry, Receptors, Neurokinin-1 analysis
- Abstract
Background and Aims: Previous immunohistochemical studies failed to reveal neurokinin (NK)(1) tachykinin receptors on intestinal muscle, despite convincing pharmacologic data indicating their presence. This study aimed to apply optimal immunohistochemical methods to reveal the receptors., Methods: NK(1)-receptor immunoreactivity was examined by confocal microscopy in tissue incubated with or without 10(-7) mol/L substance P (SP), 10(-7) mol/L SP plus 10(-6) mol/L NK(1) receptor antagonist (CP99994), or with fluorescent cyanine 3.18 (Cy3) SP., Results: Without incubation, NK(1)-receptor immunoreactivity was strong on muscle of the rectum and distal colon and weak in proximal colon and small intestine. NK(1) receptor was located on the surface of muscle cells in all gut regions. Exposure to SP increased the intensity of immunoreactivity, and the receptor moved into the cytoplasm. Mobilization of the receptor by SP was blocked by the NK(1)-receptor antagonist CP99994. Cy3-SP was internalized by muscle cells and colocalized with the receptor. NK(1)-receptor immunoreactivity occurred on crypt epithelial cells in the small intestine and the base of glands in the proximal colon., Conclusions: The NK(1) receptor occurs on the external muscle throughout the small and large intestines. SP binds and triggers NK(1)-receptor aggregation and internalization in the muscle.
- Published
- 2001
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5. Effects of very low dose daily, long-term aspirin therapy on gastric, duodenal, and rectal prostaglandin levels and on mucosal injury in healthy humans.
- Author
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Cryer B and Feldman M
- Subjects
- Adult, Aged, Aged, 80 and over, Aspirin adverse effects, Aspirin therapeutic use, Cyclooxygenase Inhibitors adverse effects, Cyclooxygenase Inhibitors therapeutic use, Dose-Response Relationship, Drug, Duodenum drug effects, Endoscopy, Digestive System, Female, Gastric Mucosa drug effects, Gastric Mucosa pathology, Humans, Intestinal Mucosa drug effects, Intestinal Mucosa metabolism, Intestinal Mucosa pathology, Male, Middle Aged, Rectum drug effects, Stomach drug effects, Thromboxane B2 blood, Time Factors, Aspirin administration & dosage, Cyclooxygenase Inhibitors administration & dosage, Duodenum metabolism, Gastric Mucosa metabolism, Prostaglandins biosynthesis, Rectum metabolism
- Abstract
Background & Aims: The safety of low-dose daily aspirin therapy in the gastrointestinal tract is uncertain. Our objectives were to evaluate the long-term effects of very low daily aspirin doses in the gastrointestinal tract and effects on platelet-derived serum thromboxane levels in volunteers., Methods: Subjects were randomized to receive 10 mg (n = 8), 81 mg (n = 11), or 325 mg (n = 10) aspirin daily for 3 months. Before administration of aspirin, all subjects underwent gastroduodenoscopy, and most underwent proctoscopy for assessment of mucosal injury and prostaglandin content. After 1.5 and 3 months, subjects again underwent gastroduodenoscopy and, at 3 months, another proctoscopy., Results: Each aspirin dose (even 10 mg) significantly reduced gastric mucosal prostaglandin levels, to approximately 40% of the baseline value. All three doses also induced significant gastric injury, and 325 mg caused duodenal injury. Three subjects developed gastric ulcers, 1 while taking 10 mg/day of aspirin. Furthermore, aspirin at 81 mg/day and 325 mg/day (but not 10 mg/day) significantly reduced duodenal mucosal prostaglandin levels to approximately 40% of the baseline value. Only 325 mg of aspirin per day significantly reduced rectal mucosal prostaglandin levels to approximately 60% of the baseline value. Serum thromboxane levels were inhibited 62%, 90%, and 98% with 10, 81, and 325 mg of aspirin., Conclusions: The findings explain aspirin's predominant gastric toxicity and question the safety of even 10 mg of aspirin daily.
- Published
- 1999
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6. Role of neurokinin 3 receptors on responses to colorectal distention in the rat: electrophysiological and behavioral studies.
- Author
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Julia V, Su X, Buéno L, and Gebhart GF
- Subjects
- Animals, Colon drug effects, Electromyography, Gastrointestinal Motility drug effects, Injections, Intraperitoneal, Injections, Intraventricular, Male, Muscle Contraction drug effects, Pain Measurement, Peptide Fragments administration & dosage, Peptide Fragments pharmacology, Piperidines administration & dosage, Piperidines pharmacology, Pressure, Rats, Rats, Sprague-Dawley, Rats, Wistar, Receptors, Neurokinin-3 agonists, Receptors, Neurokinin-3 antagonists & inhibitors, Rectum drug effects, Sensory Thresholds, Substance P administration & dosage, Substance P analogs & derivatives, Substance P pharmacology, Visceral Afferents drug effects, Visceral Afferents physiology, Colon physiology, Receptors, Neurokinin-3 physiology, Rectum physiology
- Abstract
Background & Aims: Tachykinins contribute to the control of gastrointestinal motility and modulation of somatic and visceral pain. The role of neurokinin (NK) B and NK3 receptors in visceral pain and gastrointestinal disorders has not been determined., Methods: Using electromyographic recordings of both abdominal and colonic muscle and electrophysiological recordings of pelvic nerve afferent fibers, we studied drug effects on responses to colorectal distention., Results: In awake rats, intraperitoneal administration of the NK3-receptor antagonist SR 142,801 reduced, whereas the NK3-receptor agonist senktide increased, both the rectocolonic inhibitory reflex and abdominal contractions produced by colorectal distention. In contrast, intracerebroventricular administration of SR 142,801 increased the number of abdominal contractions without affecting the rectocolonic inhibitory reflex produced by colorectal distention. In a similar manner, intracerebroventricular injection of senktide diminished the number of abdominal contractions. In electrophysiological experiments, SR 142,801 decreased responses of pelvic nerve afferent fibers to colorectal distention. Responses of pelvic nerve fibers to urinary bladder distention, however, were unaffected by SR 142,801., Conclusions: These results suggest that peripheral NK3 receptors are involved in the mediation of both visceral nociception and gastrointestinal disorders. Also, central NK3 receptors seem to play a role in the modulation of visceral nociception.
- Published
- 1999
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7. Wheat bran suppresses potato starch--potentiated colorectal tumorigenesis at the aberrant crypt stage in a rat model.
- Author
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Young GP, McIntyre A, Albert V, Folino M, Muir JG, and Gibson PR
- Subjects
- Analysis of Variance, Animals, Cell Count drug effects, Cell Cycle drug effects, Colon drug effects, Colon pathology, Colorectal Neoplasms chemically induced, Colorectal Neoplasms pathology, Dimethylhydrazines, Disease Models, Animal, Epithelium drug effects, Epithelium pathology, Precancerous Conditions chemically induced, Precancerous Conditions pathology, Random Allocation, Rats, Rectum drug effects, Rectum pathology, Carcinogens toxicity, Colorectal Neoplasms prevention & control, Dietary Fiber pharmacology, Precancerous Conditions prevention & control, Solanum tuberosum, Starch toxicity
- Abstract
Background & Aims: Starch that escapes digestion in the small intestine (resistant starch [RS]) may act similarly to nonstarch polysaccharides in the colon. The aim of this study was to examine the effect of raw potato starch alone and in combination with wheat bran on tumor development and precancer events in a rat model of colorectal cancer., Methods: Three groups of rats received either a low-RS/low-fiber ("basic") diet, the basic diet containing raw potato starch as 20% of carbohydrate content, or the potato starch diet plus 10% of "wheat bran" fiber. Epithelial proliferation, aberrant crypt foci (ACF), and tumors were measured 6 and 20 weeks after a 10-week course of dimethylhydrazine., Results: Rats on the potato starch diet had tumors more frequently and had larger tumors than rats consuming the wheat bran or basic diets. Parallel effects on the density of ACF were found 6 weeks after the carcinogen. Although epithelial proliferation was significantly enhanced by potato starch compared with the basic diet, the addition of wheat bran did not suppress this enhancement., Conclusions: This type-2 RS enhances epithelial proliferation, ACF density, and tumor formation. The addition of wheat bran to an RS-containing diet suppresses tumorigenesis, acting on events responsible for the formation of ACF but not the events controlling the hyperproliferative phase.
- Published
- 1996
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8. The effects of sulindac on colorectal proliferation and apoptosis in familial adenomatous polyposis.
- Author
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Pasricha PJ, Bedi A, O'Connor K, Rashid A, Akhtar AJ, Zahurak ML, Piantadosi S, Hamilton SR, and Giardiello FM
- Subjects
- Adenomatous Polyposis Coli immunology, Adenomatous Polyposis Coli pathology, Adult, Analysis of Variance, Apoptosis drug effects, Cell Cycle drug effects, Cell Division drug effects, Colon immunology, Colon pathology, Double-Blind Method, Epithelium drug effects, Epithelium immunology, Epithelium pathology, Female, Flow Cytometry, Humans, Immunohistochemistry, Male, Middle Aged, Multivariate Analysis, Proliferating Cell Nuclear Antigen analysis, Rectum immunology, Rectum pathology, Remission Induction, Adenomatous Polyposis Coli drug therapy, Colon drug effects, Rectum drug effects, Sulindac therapeutic use
- Abstract
Background & Aims: The mechanism by which sulindac causes regression of adenomas in patients with familial adenomatous polyposis (FAP) is unclear. Conflicting data on the drug's effects on colorectal epithelial proliferation have been reported. An alternative mechanism, and one not previously studied, is via induction of colorectal epithelial cell apoptosis (programmed cell death). This hypothesis was tested by studying the effects of sulindac on colorectal epithelial proliferation and apoptosis in patients with FAP., Methods: Cell proliferation was studied via immunohistochemistry for cell nuclear antigen in a group of 22 patients randomized to either sulindac (150 mg twice a day) or placebo in a previously published trial. The rectal epithelium from 7 additional patients with FAP treated with sulindac was examined by flow cytometry to assess changes in cell-cycle distribution and apoptosis., Results: Although sulindac caused a significant decrease in polyp size and number, there was no significant change in cytokinetic variables or cell cycle distribution 3 months after treatment. However, the subdiploid apoptotic fraction was increased significantly 3 months after treatment with sulindac (31.3% +/- 4.8% compared with 10% +/- 4.3% at baseline; P = 0.01)., Conclusions: Our findings suggest that sulindac does not affect colorectal epithelial proliferation and that its effects in patients with FAP may instead result from induction of apoptosis.
- Published
- 1995
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9. Omega-3 fatty acids and rectal epithelial cell proliferation.
- Author
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Newmark H and Lipkin M
- Subjects
- Adenomatous Polyposis Coli diet therapy, Adenomatous Polyposis Coli pathology, Calcium, Dietary administration & dosage, Cell Division drug effects, Dietary Fiber administration & dosage, Epithelium drug effects, Epithelium pathology, Fatty Acids, Omega-3 administration & dosage, Fish Oils administration & dosage, Fish Oils therapeutic use, Humans, Rectum pathology, Fatty Acids, Omega-3 therapeutic use, Rectum drug effects
- Published
- 1994
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10. Evidence for the hypersensitivity of lumbar splanchnic afferents in irritable bowel syndrome.
- Author
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Lembo T, Munakata J, Mertz H, Niazi N, Kodner A, Nikas V, and Mayer EA
- Subjects
- Adult, Catheterization, Compliance, Female, Humans, Lidocaine pharmacology, Lumbosacral Region, Male, Middle Aged, Perception, Rectum drug effects, Rectum physiopathology, Sensation, Sensory Thresholds, Afferent Pathways physiopathology, Colonic Diseases, Functional physiopathology, Spinal Cord physiopathology, Splanchnic Nerves physiopathology
- Abstract
Background/aims: The pathways underlying rectal hypersensitivity to balloon distention in patients with irritable bowel syndrome (IBS) are not known. The aim of this study was to characterize the involvement of sacral and thoracolumbar afferents in the perception of rectal distention., Methods: Rectal balloon distention was performed in 15 normal control subjects, 6 patients with spinal cord injury, and 50 patients with IBS using a slow-volume ramp (40 mL/min) or rapid phasic step distension. Additional studies were performed in the presence of 2% intrarectal lidocaine., Results: Patients with spinal cord injury with lesions below T7 reported sensations only during phasic distention. Sixty percent of patients with IBS (n = 50) were hypersensitive for discomfort during phasic distention, whereas only 4% were hypersensitive during ramp distention. Less than 15% of patients were hypersensitive for the sensation of stool. In normal patients, lidocaine increased thresholds in response to slow ramp distention by 40%-70% but had no effect on perception in response to other types of distention. Lidocaine had no effect on (1) thresholds in response to either ramp or phasic distention in normosensitive or hypersensitive patients with IBS or (2) the rate of receptive relaxation or rectal compliance in any group., Conclusions: Rapid phasic distention preferentially stimulates splanchnic afferents. Hypersensitivity of these afferents in patients with IBS is unaffected by mucosally applied lidocaine.
- Published
- 1994
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11. Enhanced thromboxane A2 and prostacyclin production by cultured rectal mucosa in ulcerative colitis and its inhibition by steroids and sulfasalazine.
- Author
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Ligumsky M, Karmeli F, Sharon P, Zor U, Cohen F, and Rachmilewitz D
- Subjects
- Epoprostenol biosynthesis, Humans, In Vitro Techniques, Mucous Membrane drug effects, Mucous Membrane metabolism, Prostaglandins E biosynthesis, Rectum drug effects, Steroids pharmacology, Colitis, Ulcerative metabolism, Prostaglandins biosynthesis, Rectum metabolism, Sulfasalazine pharmacology, Thromboxane A2 biosynthesis, Thromboxanes biosynthesis
- Abstract
Accumulation of 6-ketoprostaglandin F1 alpha and thromboxane B2, the stable metabolites of prostacyclin I2 and thromboxane A2 respectively, by cultured rectal mucosa obtained from patients with active ulcerative colitis was significantly higher than their respective accumulation by cultured biopsy specimens obtained from normal subjects. Accumulation of prostacyclin I2 and thromboxane A2 by rectal mucosa obtained from ulcerative colitis patients in remission was not enhanced. Prostacyclin I2, thromboxane A2, and prostaglandin E2 accumulation was significantly inhibited by the addition to the culture medium of 5-aminosalicylic acid, flufenamic acid, aspirin, azathioprine, and methylprednisolone. Sulfapyridine inhibited significantly only prostaglandin E2 and prostacyclin I2 while sulfasalazine inhibited thromboxane A2, prostaglandin E2, and prostacyclin I2 accumulation. Flufenamic acid potentiated the inhibition of prostaglandin E2 accumulation induced by methylprednisolone when administered alone. These results suggest that in addition to the mediation by prostaglandin E2, thromboxane A2 and prostacylin I2 may also be involved in the inflammatory response in ulcerative colitis. Moreover, the therapeutic effects of steroid hormones and sulfasalazine may be partially related to their inhibition of colonic prostaglandin E2, prostacyclin I2, and thromboxane A2 synthesis.
- Published
- 1981
12. Mechanism of the excitatory action of motilin on isolated rabbit intestine.
- Author
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Adachi H, Toda N, Hayashi S, Noguchi M, Suzuki T, Torizuka K, Yajima H, and Koyama K
- Subjects
- Acetylcholine physiology, Animals, Calcium pharmacology, Duodenum drug effects, Ileum drug effects, Muscle Contraction drug effects, Muscle, Smooth drug effects, Rabbits, Rectum drug effects, Verapamil pharmacology, Gastrointestinal Hormones pharmacology, Gastrointestinal Motility drug effects, Motilin pharmacology
- Abstract
Synthetic motilin caused a dose-dependent contraction on isolated rabbit intestinal segments, including the duodenum, ileum, and rectum. The contraction of duodenum was significantly greater than that in the ileum or rectum. In the duodenum, motilin was approximately 100 times as potent as acetylcholine on molar basis. The motilin-induced contractions were not influenced by atropine, chlorpheniramine, cimetidine, phentolamine, propranolol, cinanserin, 1-sar-8-ala-angiotensin II, or aspirin. Motilin did not affect the contraction induced by transmural electrical stimulation or acetylcholine. The response to motilin was unaffected by acetylcholine. Removal of Ca++ from bathing media or verapamil suppressed the motilin-induced contractions to a significantly greater extent than the contractions induced by acetylcholine. Thus, it may be concluded that motilin produces intestinal contractions by acting directly on smooth muscles, but not by acting on pharmacologically known drug receptors nor by releasing neurotransmitters such as endogenous acetylcholine. Motilin does not appear to modify autonomic nerve functions.
- Published
- 1981
13. Human rectal mucosa: proctoscopic and morphological changes caused by laxatives.
- Author
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Meisel JL, Bergman D, Graney D, Saunders DR, and Rubin CE
- Subjects
- Bisacodyl adverse effects, Enema adverse effects, Humans, Intestinal Mucosa pathology, Intestinal Mucosa ultrastructure, Mannitol adverse effects, Proctoscopy, Rectum pathology, Rectum ultrastructure, Sodium Chloride adverse effects, Cathartics adverse effects, Intestinal Mucosa drug effects, Rectum drug effects
- Abstract
To determine whether laxatives alter the proctoscopic and morphological appearances of the human rectum, 10 normal subjects were studied prospectively, and the following manipulations were assessed in a randomized, blinded manner: no treatment; oral mannitol to induce diarrhea; isotonic saline enema; Fleet's Phospho-Soda enema; and bisacodyl (Dulcolax), 10 mg, by enema or suppository. The rectal mucosa after mannitol-induced diarrhea, or after saline enema could not be distinguished from untreated rectum by proctoscopy, light microscopy, or scanning electron microscopy. Fleet's enema, and bisacodyl invariably changed proctoscopic appearances, and frequently altered light and scanning microscopic aspects. Both Fleet's enema and bisacodyl caused sloughing of surface epithelium. In addition, bisacodyl decreased the uptake of hematoxylin and eosin by crypt epithelial cells so that the affected cells had a partially erased appearance (16 of 25 biopsies examined by light microscopy). The lamina propria of 3 of these 25 biopsies contained polymorphonuclear cells. Transmission electron microscopy revealed that the abnormal crypt epithelial cells contained fewer cytoplasmic organelles and less nuclear chromatin. All lesions resolved within 7 days. Fleet's enema and bisacodyl by rectum may mislead the proctologist and the pathologist by altering normal rectal mucosa.
- Published
- 1977
14. Effect of laxatives on human rectal mucosa.
- Author
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Dantas W
- Subjects
- Humans, Sigmoidoscopy, Cathartics pharmacology, Intestinal Mucosa drug effects, Rectum drug effects
- Published
- 1978
15. Role of clostridial toxin in the pathogenesis of clindamycin colitis in rabbits.
- Author
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LaMont JT, Sonnenblick EB, and Rothman S
- Subjects
- Administration, Oral, Animals, Antitoxins administration & dosage, Antitoxins therapeutic use, Colitis microbiology, Colitis prevention & control, Feces analysis, Injections, Intraperitoneal, Intestinal Mucosa drug effects, Intestinal Mucosa pathology, Rabbits, Rectum drug effects, Rectum pathology, Bacterial Toxins administration & dosage, Bacterial Toxins analysis, Clindamycin administration & dosage, Clostridium pathogenicity, Colitis chemically induced
- Abstract
The pathophysiology of antibiotic-associated colitis was studied in rabbits with severe ileocolitis induced by oral administration of clindamycin. Cell-free, sterile filtrates of cecal contents of rabbits with clindamycin colitis contained a toxin that was lethal for mice and cytotoxic for HeLa-cell monolayers. The toxin was heat labile, was inactivated by pronase but not trypsin, and had a mol wt by gel filtration on Sephadex G-100 of 45,000. The toxin was neutralized by antiserum to Clostridium perfringens type E, but not by other clostridial antisera. The toxin also caused severe necrosis of rabbit rectal epithelium during 18-hr organ culture, which could be completely reversed by neutralization with C. perfringens type E antiserum. These studies indicate that clindamycin colitis in rabbits is caused by overgrowth of a clostridial species, which releases a heat-labile toxic protein of mol wt of 45,000 capable of necrosing colonic epithelial cells.
- Published
- 1979
16. Studies of intestinal lymphoid tissue. XII. Epithelial lymphocyte and mucosal responses to rectal gluten challenge in celiac sprue.
- Author
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Loft DE, Marsh MN, Sandle GI, Crowe PT, Garner V, Gordon D, and Baker R
- Subjects
- Adult, Aged, Capillary Permeability drug effects, Female, Humans, Intestinal Mucosa blood supply, Intestinal Mucosa pathology, Male, Mast Cells ultrastructure, Microscopy, Electron, Middle Aged, Rectum drug effects, Celiac Disease pathology, Glutens pharmacology, Intestinal Mucosa drug effects
- Abstract
The immunopathologic, structural, and functional changes within rectal mucosa of known celiac sprue subjects were quantitated during local challenge with a peptic-tryptic digest of gluten. In the celiac sprue patients challenged with 2 g of digest, major effects occurred in lamina propria, submucosa, and local microvasculature. The lamina propria swelling was biphasic, starting 1-2 h after challenge with widespread extravascular deposition of fibrinogen, indicative of increased microvascular permeability, receding by 24 h postchallenge. A rapid fall in mast cells together with granule discharge suggested their involvement in this response. The late-phase swelling (48-72 h) was preceded by a rapid influx of neutrophils and basophils, the latter showing evidence of degranulation beyond 72 h. Reestablishment of vessel lumina, a rise in mast cells, and loss of neutrophils indicated tapering of the inflammatory cellular cascade by 96 h. Lymphocytes, first seen to enter the lamina by 2 h postchallenge, increased progressively, thereby resulting in substantial infiltration between 36 and 96 h. A marked rise in epithelial lymphocytes, maximal at 6-8 h, waned by 24 h. Volumes of surface and crypt epithelium remained constant throughout. In another challenge series with 4 g of gluten digest, electrical potential difference across rectal mucosa decreased significantly 12 h postchallenge, but the associated decreases in net sodium and chloride absorptive fluxes were insignificant. It is concluded that rectal mucosa is sensitized to gluten in celiac sprue disease and thus offers a promising and convenient in vivo substrate for investigative and diagnostic purposes.
- Published
- 1989
- Full Text
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17. Effects of topical 5-aminosalicylic acid and prednisolone on prostaglandin E2 and leukotriene B4 levels determined by equilibrium in vivo dialysis of rectum in relapsing ulcerative colitis.
- Author
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Lauritsen K, Laursen LS, Bukhave K, and Rask-Madsen J
- Subjects
- Adult, Aged, Clinical Trials as Topic, Colitis, Ulcerative metabolism, Dialysis, Dinoprostone, Double-Blind Method, Enema, Female, Humans, Intestinal Mucosa metabolism, Male, Mesalamine, Middle Aged, Random Allocation, Rectum drug effects, Aminosalicylic Acids therapeutic use, Colitis, Ulcerative drug therapy, Leukotriene B4 metabolism, Prednisolone therapeutic use, Prostaglandins E metabolism
- Abstract
To determine the influence of inflammation and topical treatment with 5-aminosalicylic acid or prednisolone on arachidonic acid metabolism in vivo, we carried out a double-blind controlled study on the release of prostaglandin E2 and leukotriene B4 to the rectal lumen in 24 consecutive patients with proven distally located ulcerative colitis. Before and at days 15 and 29 a dialysis bag was placed in the emptied rectum for 4 h prior to assessing clinical, endoscopic, and histologic disease activity. A single enema was given daily at bedtime (1 g 5-aminosalicylic acid or 25 mg prednisolone) until complete remission or for a maximum of 4 wk. Clinical and endoscopic remission was obtained in 16 (7 on 5-aminosalicylic acid) and 11 (3 on 5-aminosalicylic acid) patients, respectively. Luminal concentrations of prostaglandin E2 and leukotriene B4 were positively correlated to disease activity and significantly decreased among the prednisolone-treated patients. In both treatment groups a decrease toward normal levels occurred in patients responding to therapy. In retrospect, the pretreatment prostaglandin E2 and leukotriene B4 levels were significantly higher in patients not responding to therapy than in those improving during treatment. In conclusion, luminal prostaglandin E2 and leukotriene B4 levels may prove more useful predictors of the outcome of treatment in relapsing ulcerative colitis than clinical indices of disease activity.
- Published
- 1986
- Full Text
- View/download PDF
18. Motor responses of the sigmoid colon and rectum to exogenous cholecystokinin and secretin.
- Author
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Dinoso VP Jr, Meshkinpour H, Lorber SH, Gutierrez JG, and Chey WY
- Subjects
- Adult, Aged, Depression, Chemical, Dose-Response Relationship, Drug, Female, Humans, Male, Middle Aged, Stimulation, Chemical, Cholecystokinin pharmacology, Colon drug effects, Gastrointestinal Motility drug effects, Rectum drug effects, Secretin pharmacology
- Published
- 1973
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