Histochemical changes in mucus in duodenal ulceration.

Morrissey, Shelagh M.; Ward, Pamela; Jayaraj, A. P.; Tovey, F I; Clark, C. G.

doi:10.1136/gut.24.10.909

Cited by 24 publications

(11 citation statements)

References 11 publications

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“…The correspondence between histological staining and core mucin polypeptide subtype (e.g., muc2, muc3, and muc6) has not yet been firmly established (12,25). Acid-induced augmentation of mixed PASand AB-positive glycoproteins suggests that increased mucus secretion and exudation originates mainly from goblet cells.…”

Section: Discussionmentioning

confidence: 99%

“…In the gastrointestinal tract, mucus secretion is generally inferred from examination of histological sections stained by the periodic acid/Schiff (PAS) or Alcian blue (AB) techniques (25,28). Secretion has also been extrapolated from measurements of mucus glycoprotein of luminal perfusates by PAS staining (24,36) or hexosamine measurement (19); mucus gel thickness (MGT) has been measured in tissue sections by the method developed by Kerss et al (14).…”

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confidence: 99%

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Dynamic regulation of mucus gel thickness in rat duodenum

Akiba¹,

Guth

Engel³

et al. 2000

American Journal of Physiology-Gastrointestinal and Liver Physi

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. Dynamic regulation of mucus gel thickness in rat duodenum. Am J Physiol Gastrointest Liver Physiol 279: G437-G447, 2000.-We examined the dynamic regulation of mucus gel thickness (MGT) in vivo in rat duodenum in response to luminal acid, cyclooxygenase (COX) inhibition, and exogenous PGE 2 . An in vivo microscopic technique was used to measure MGT with fluorescent microspheres in urethan-anesthetized rats. Duodenal mucosa was topically superfused with pH 7.0 or pH 2.2 solutions with or without PGE 2 and indomethacin treatments. Glycoprotein concentration of duodenal loop perfusates was measured with periodic acid/Schiff (PAS) or Alcian blue (AB) staining. MGT and perfusate glycoprotein concentration were stable during a 35-min perfusion with pH 7.0 solution. Acid exposure increased MGT and PAS-and ABpositive perfusate glycoprotein concentrations. Indomethacin pretreatment increased both PAS-and AB-positive perfusate glycoprotein at baseline; subsequent acid superfusion decreased perfusate glycoproteins and gel thickness. PGE 2 (1 mg/kg iv) simultaneously increased MGT and PAS-positive perfusate glycoprotein concentrations followed by a transient increase in AB-positive glycoprotein concentration, suggesting contributions from goblet cells and Brunner's glands. Parallel changes in MGT and perfusate glycoprotein concentration in response to luminal acid and PGE 2 suggest that rapid MGT variations reflect alterations in the balance between mucus secretion and exudation, which in turn are regulated by a COX-related pathway. Luminal acid and PGE 2 augment mucus secretion from goblet cells and Brunner's glands. fluorescent microspheres; perfusate glycoprotein concentration; indomethacin; periodic acid/Schiff staining; Alcian blue staining; Brunner's glands THE PROXIMAL DUODENAL MUCOSA is exposed to frequent pulses of gastric acid. Unlike other acid-exposed organs such as the stomach or esophagus, the duodenum is functionally "leaky" in that the epithelial cell layer is an incomplete barrier to solute diffusion, increasing the importance of nonstructural defense mechanisms such as the mucus gel layer, bicarbonate secretion, and blood flow. The viscoelastic mucus gel layer is the first line of defense against luminal contents and is thought to play an important role in decreasing mucosal injury due to acid. Mucus secretion is increased by luminal acid (19, 33) and the neuro-and inflammatory mediators acetylcholine and interleukin-1 (8), vasoactive intestinal polypeptide (15), secretin (16,19), and guanylin (10) in duodenum. In the stomach and intestine, mucus secretion and gel thickness are increased by prostaglandins (5, 20, 24, 36), pentagastrin (26, 45), carbachol (30, 31), nitric oxide (7, 30), bradykinin (41) and phorbol esters (29). Of these factors, prostaglandins, products of the cyclooxygenase (COX) pathway, are of paramount clinical importance, because COX inhibition is an important cause of clinical duodenal ulceration (38).In the gastrointestinal tract, mucus secretion is generally inferred from examinatio...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Dynamic regulation of mucus gel thickness in rat duodenum

Akiba¹,

Guth

Engel³

et al. 2000

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…The addition of sucralfate to 'damaged' mucus reestablishes its ability to act as an ion exchange membrane (17). In peptic ulcer disease the composition of mucus and its thickness are altered (M), and its production reduced (19). The potential of drug therapy to improve the mucus barrier is in its infancy.…”

Section: Mucus Hco Mucinsmentioning

confidence: 99%

Pathogenesis of Peptic Ulcer Disease and Gastritis: Importance of Aggressive and Cytoprotective Factors

Tasman-Jones

1986

Scandinavian Journal of Gastroenterology

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Tasman-Jones C. Pathogenesis of peptic ulcer disease and gastritis: importance of aggressive and cytoprotective factors. Scand J Gastroenterol 1986, 2l(suppl 122), Acid production is a major gastric function. Second messengers (cyclic AMP and calcium) are released when parietal cell membrane receptors (Hz, muscarinic and gastrin) are stimulated. The second messengers then stimulate the 'gastric proton pump' to produce hydrogen ions. New evidence suggests that there is a unidirectional flux of hydrogen ions into the lumen induced by unique physical properties of mucus and a sodium gradient from lumen to serosa. Luminal hydrogen ions, bile salts, ingested drugs, and ingested alcohol are potential gastric epithelial toxins. The stomach's protective mechanism includes a well-defined mucus layer, an epithelial bicarbonate secretion, a tight epithelium, and a good nutrient blood supply. Endogenous prostaglandins partly control these mechanisms. Modern therapeutics are increasingly directed towards improving gastric cytoprotection.

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“…Groups 2, 3, and 4 (40 rats each) received intragastric instillation of NaOH solution by Oohara's method7 as previously modified by us.6 Briefly, the rats were starved for 48 hours, then the abdomen was opened and the stomach raised. The oesophagus and duodenum were clamped from the outside with arterial clamps 2 cm from the gastric pylorus, and 3*0 ml of 5% NaOH solution was injected into the stomach with a fine needle (outside diameter, 0-5 mm) inserted through the forestomach.…”

Section: Animallsmentioning

confidence: 99%

Enhancement by tetragastrin of experimental induction of gastric epithelium in the duodenum.

Tatsuta

Yamamura

Yamamoto

et al. 1989

Gut

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SUMMARY The effects of tetragastrin and truncal vagotomy on the incidence of gastric type epithelium in the duodenum by intraduodenal instillation of 5% NaOH solution were investigated in Wistar rats. Prolonged administration of 1 mg tetragastrin/kg body weight in depot form starting one week after NaOH treatment resulted in a significant increase in gastric acid secretion and the incidence and number of villi with gastric epithelium in the duodenum in experimental week 10. Villi with gastric epithelium were found in five (23%) of 22 rats in control group, whereas abnormal villi were found in 13 (59%) of 22 rats in the tetragastrin treated group (p<005). The average number of villi with gastric epithelium rose from 0-6 (0O4) per 100 villi in control rats to 2-4 (0-6) per 100 villi in tetragastrin treated rats (p<0O01). On histological examination, gastric type epithelium was most often found on stunted or flattened villi, and was always within the boundaries of the area of Brunner's glands. These mucosal changes reverted toward normal with time. In week 35, the incidence of gastric epithelium was significantly less than at week 10 (p<005). In contrast, no villi with gastric epithelium were found in vagotomised rats in week 10 (p<005). Vagotomy also caused a significant decrease in gastric acid secretion. These results show that exposure of the duodenal mucosa to high levels of gastric acid enhance the induction of gastric epithelium in the duodenum.In 1964 James described the partial replacement of the normal epithelial cells of the human duodenal mucosa by epithelial calls containing mucus.' Since then, gastric type epithelium has frequently been seen in patients with duodenal ulcer2 and duodenitis.'These mucosal changes are thought to constitute a protective mechanism, involved in some way with ulcer healing.4 The histogenesis of these changes, however, is still under discussion.In 1964, Rhodes reported that the administration of histamine induced gastric type epithelium in the duodenum of the cat.' We recently reported that prolonged administration of tetragastrin decreased the incidence and number of intestinal metaplasias induced by intragastric instillation of NaOH solution in rats.6 In the present work, we applied this method to the duodenum, and examined the effect of tetraAddress for correspondence: Dr Masaharu Tatsuta. Department of Gastrointestinal Oncology. The Center for Adult Diseases. Osaka 3-3. Nakamichi 1-chome. Higashinari-ku. Osaka 537. Japan. Accepted for publication 25 August 1988. 311 gastrin on the production of gastric epithelium in the duodenum. Methods ANIMALLSWe used 155 six week old male inbred Wistar rats weighing 100-120 g. The rats were randomly divided into four groups, and treated as follows.Groups 2, 3, and 4 (40 rats each) received intragastric instillation of NaOH solution by Oohara's method7 as previously modified by us.6 Briefly, the rats were starved for 48 hours, then the abdomen was opened and the stomach raised. The oesophagus and duodenum were clamped from the outsid...

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Histochemical changes in mucus in duodenal ulceration.

Cited by 24 publications

References 11 publications

Dynamic regulation of mucus gel thickness in rat duodenum

Dynamic regulation of mucus gel thickness in rat duodenum

Pathogenesis of Peptic Ulcer Disease and Gastritis: Importance of Aggressive and Cytoprotective Factors

Enhancement by tetragastrin of experimental induction of gastric epithelium in the duodenum.

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