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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 38 (1993), S. 1450-1452 
    ISSN: 1573-2568
    Keywords: nicotine ; smoking ; prostaglandins ; gastric mucosa
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previous studies have shown that cigarette smoking depresses prostaglandin generation by human gastric mucosa, but the component of smoke that is responsible for that action is not known. To investigate whether nicotine has a direct effect on gastric mucosal prostaglandin generation, we performed the following study. Eight rats were sacrificed and the stomachs removed. Using a biopsy forceps, small pieces of gastric mucosa were resected and placed in incubation vials containing either buffered Krebs solution alone (control), Krebs solution plus indomethacin (5 μg/ml), or Krebs solution plus one of several concentrations of nicotine ditartrate (10, 100, 500, 1000 ng/ml). The nicotine concentrations we used ranged below and above the plasma nicotine concentrations of smokers shortly after smoking cigarettes. Three separate incubations of gastric mucosa were performed per experimental group from each animal. After 30 min of incubation, prostaglandin E2 and 6-keto-prostaglandin F1α concentrations in the incubation medium were measured by radioimmunoassay. We found that nicotine at any concentration tested had no effect on the generation of prostaglandin E2 and 6-keto-prostaglandin F1α by rat gastric mucosa. Thus, this study indicates that, if nicotine is involved in the depression of prostaglandin generation in the gastric mucosa of smokers, its role is an indirect one and not by direct action on the gastric mucosa.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 28 (1983), S. 61-64 
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recent reports of the association of cimetidine treatment with the development of gastric carcinoma stimulated us to study the effect of chronic cimetidine ingestion on epithelial proliferation in the stomach of male Wistar/Lewis rats. One group of rats received cimetidine in the drinking water to deliver 150–200 mg/kg/day. Control rats received plain water. To label proliferating cells, the rats were injected by tail vein with tritiated thymidine 1 hr before sacrifice at 1, 6, and 12 months. Sections of fundus and antrum were processed for light autoradiography. We found no histological evidence for malignant change and no effect on the measurements of epithelial proliferation by cimetidine in either fundus or antrum at any of the times studied, with the possible exception of an upward shift in the distribution of labeled cells within the proliferative zone of the fundus after 6 months. Thus, under the conditions of our experiments we have been unable to identify an effect of cimetidine on epithelial proliferation which would implicate it as a chemical carcinogen.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-2568
    Keywords: Helicobacter pylori ; gastroduodenal mucosa ; prostaglandins ; bismuth subsalicylate ; Pepto-Bismol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To determine whetherHelicobacter pylori has an effect on gastroduodenal mucosal prostaglandin generation, mucosal biopsies were obtained from the gastric body, antrum, and duodenal bulb of 30 patients who were undergoing upper gastrointestinal endoscopy for clinical indications. One biopsy from the gastric body and one from the antrum were tested for urease activity (urea broth) and one biopsy from each area including the duodenum was processed for histology. Two other biopsies form each area were incubated and the accumulation of prostaglandin E2 and 6-keto prostaglandin F1α in the incubation medium was measured by radioimmunoassay. Twelve of the 17H. pylori-positive patients and seven of the 13H. pylori-negative patients agreed to take bismuth subsalicylate (Pepto-Bismol) two tablets four times a day for four weeks. One week after treatment, these patients again underwent endoscopy and the above studies. This study indicates that: (1) mucosal PGE2 generation may be increased in the duodenum, gastric body, and antrum inH. pylori-positive patients compared toH. pylori-negative patients, and (2) treatment with bismuth subsalicylate for four weeks results in reduction of mucosal PGE2 in the duodenum, gastric body, and antrum ofH. pylori-positive patients and fails to eradicateH. pylori or reduce gastric inflammation.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 33 (1988), S. 1064-1069 
    ISSN: 1573-2568
    Keywords: hydrocortisone ; corticosteroids ; epithelial renewal ; epithelial proliferation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of this study was to determine whether parenteral administration of steroids affects epithelial renewal in hamster stomach. Male golden hamsters received either hydrocortisone sodium succinate or saline intraperitoneally for three days. In the first experiment, hamsters were sacrificed 1 hr after injection of tritiated thymidine ([3]HTdR) to label proliferating cells. In the second experiment, hamsters were sacrificed hourly after a single [3H]TdR injection up to 48 hr in order to determine cell cycle time by the method of fraction of labeled mitoses. In the third experiment, hamsters were sacrificed 1, 24, and 72 hr after [3H]TdR injection for the study of epithelial migration and cell turnover time. Sections of fundic and antral mucosae were prepared for light autoradiography. Steroid treatment caused no gross or microscopic injury to gastric mucosa, but the number of [3H]TdR-labeled cells as well as the thickness of the proliferative zone were reduced significantly in fundic mucosa, but not in antral mucosa. The study of the fraction labeled mitoses indicated that steroid treatment lengthened the cell cycle time in fundic mucosa, which was due primarily to prolonged G1 and DNA synthesis phases. Furthermore, epithelial migration was significantly slower in fundic mucosa after steroid treatment, which was associated with a prolonged cell turnover time. Thus, parenteral steroids depress the entire process of epithelial renewal in hamster fundic mucosa.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 23 (1978), S. 429-435 
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We correlated changes in the gastric transmucosal potential difference (PD), as an indicator of the integrity of the gastric mucosal barrier, with morphological evidence of injury in dogs which had received either intragastric saline or 5, 10, 15, or 30% ethanol. Increasing degrees of morphological damage were accompanied by greater, more rapid changes in PD. Furthermore, ultrastructural changes occurred within surface epithelial cells, not in the deeper parietal or zymogen cells, and initially did not involve disruption of the apical cell membrane. Typically, the tight junctions also were not affected, although in a minority of dogs small bleblike separations of the tight junctions were seen. We consider the gastric mucosal barrier to be represented morphologically by the interconnecting sheet of gastric epithelial cells and that ethanol breaks the barrier by first causing intracellular injury.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 29 (1984), S. 498-501 
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We treated four patients who had early gastric carcinoma with weekly endoscopic local injections of 5-fluorouracil (5FU). In all four patients the lesions disappeared by endoscopic and biopsy examination within 12–18 weeks of treatment. None of the patients experienced side effects which are usually associated with oral or intravenous administration of 5FU. Two patients eventually underwent surgery. In one, a small focus of carcinoma was identified within the resected stomach; no evidence of carcinoma was found in the other. The remaining two patients have not submitted to surgery and are free of carcinoma by endoscopy for over 1 1/2 years. In this uncontrolled study, endoscopic local injection of 5FU appeared to be effective in treating early gastric carcinoma as assessed by endoscopic and histological criteria. Surgery remains the treatment of choice for early gastric carcinoma. However, further studies of endoscopic injection therapy are needed to determine whether this treatment is appropriate for patients with early gastric carcinoma who are not surgical candidates.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 30 (1985), S. 95S 
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Agents such as ethanol, aspirin, bile acids, and hypertonic urea and glucose, are capable of breaking the physiological gastric mucosal barrier and may cause ultrastructural injury to the epithelial cells within several minutes of exposure. Ethanol at any pH, and aspirin and bile acids at acid pH, are lipid soluble and diffuse rapidly into surface epithelial cells where a sequence of injury can be documented by electron microscopy. First, the nuclear chromatin becomes clumped and the density of the cytoplasmic ground substance decreases. Second, mitochondria become swollen and the apical cell membrane is distorted. Finally, the apical, cell membrane ruptures and the cell disintegrates. Throughout this sequence, the tight junctions between cells appear morphologically intact. In contrast to lipid soluble agents, hypertonic urea and glucose do not diffuse well into surface epithelial cells. Although these agents also cause rapid changes in transmucosal potential difference and ion fluxes, their ultrastructural effects are quite different. Hypertonic urea and glucose initially cause small blebs within the tight junctions and larger vacuoles within the cytoplasm of surface epithelial cells, while the remainder of the cell structure appears normal. More severe injury is characterized by more vacuolization and eventual disruption of epithelial cells. These changes presumably are secondary to osmotic shifts of fluid and electrolytes. Although the ‘cytoprotective’ effects of prostaglandins have been well described, there is virtually no information at the ultrastructural level concerning the protective effects of prostaglandins with regard to these ulcerogenic agents.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 26 (1981), S. 601-608 
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Acid-induced esophageal injury in the cat, produced by infusion of 0.1 N HCl (1 ml/min for 30 min) on 4 consecutive days, has been shown previously to adversely affect lower esophageal sphincter (LES) pressure. We studied the role of prostaglandins in acid-induced esophagitis and the associated LES hypotension by simultaneous treatment of some animals with indomethacin (150 μg/kg intravenous), a specific inhibitor of prostaglandin synthesis, either during production of esophagitis or during recovery. LES pressures and esophageal histology were compared to control groups which received acid alone. Indomethacin treatment resulted in more rapid healing of the esophageal inflammation and prevented or promptly corrected the esophagitis-associated LES hypotension. These studies provide further evidence that prostaglandins play an important role in the pathogenesis of acid-induced esophagitis and LES hypotension and raise the possibility that indomethacin, a prostaglandin synthetase inhibitor, may be of benefit in prevention or therapy of esophagitis.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 26 (1981), S. S22 
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Eighteen opossums received 2250 rad60Co to the entire esophagus and lower esophageal sphincter. Animals received treatment with 600 mg aspirin, 25 mg/kg hydrocortisone, or saline before irradiation and twice daily for 1 week after irradiation. At 10 days postirradiation, animals were evaluated for signs of acute esophagitis by esophagoscopy and barium esophagram. Each animal was then killed and the esophagus removed and evaluated histologically. Animals treated with either aspirin or hydrocortisone had significantly milder esophagitis than control irradiated animals.
    Type of Medium: Electronic Resource
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