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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 45 (1996), S. 370-375 
    ISSN: 1420-908X
    Keywords: Propranolol ; Gastric damage ; Ethanol ; Indomethacin ; Stress
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Although propranolol has been shown to protect against enthanol and stress ulceration, the antiulcer mechanisms are still unclear. The present study examined the antiulcer mechanisms of propranolol in three different types of ulceration induced respectively by ethanol (60%), indomethacin (30 mg/kg) and stress (cold-restraint). Propranolol pretreatment in the highest dose (10 mg/kg) given either intraperitoneally (i.p.) or orally (p.o.) prevented gastric mucosal damage in these three ulcer models. The three doses of the drug (2.5, 5 or 10 mg/kg) dose-dependently decreased systemic blood pressure which was accompanied by a reduction of gastric mucosal blood flow. These findings suggest that the protection was unrelated to an improvement of local circulation in the stomach. However, propranolol preserved the mucus levels in the three types of ulcer models. The β-adrenoceptor blocker also increased the basal gastric mucosal potential difference. These findings indicate that propranolol strengthens the mucosal barrier by the preservation of mucosal mucus and enhancement of the mucosal integrity in the stomach.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1420-908X
    Keywords: Mild irritants ; Ethanol ; Gastric lesions ; Gastric emptying rate ; Mucosal folds
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study examines the involvement of gastric emptying and mucosal folds in the adaptive cytoprotection of different mild irritants against 100% ethanolinduced gastric mucosal damage. Pre-exposure to either 20% ethanol, 5% NaCl or 0.3M HCl significantly reduced the gastric mucosal damage caused by 100% ethanol in rats. Administration of either one of the three mild irritants increased the basal gastric residual volume and decreased the area occupied by gastric mucosal folds, but only 20% ethanol reduced the gastric emptying rate. Indomethacin (5 mg/kg, s.c.) pretreatment did not affect ethanol ulceration and gastric emptying rate when given by itself, but reversed the flattening of mucosal folds produced by the three mild irritants, and abolished the protective effect of 20% ethanol. These results suggest that the gastric adaptive cytoprotection induced by the three mild irritants acts through luminal dilution of the noxious agent, possibly caused by gastric retention. The reduction of mucosal folds could also contribute to the anti-lesion action of 20% ethanol. It is therefore suggested that the protective actions of the three mild irritants act through different mechanisms.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 35 (1990), S. 1334-1339 
    ISSN: 1573-2568
    Keywords: adenosine ; theophylline ; ethanol ; gastric secretion ; gastric lesions ; gastric mucosal blood flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study examines the gastric effects of adenosine and its antagonist, theophylline, on secretory function, mucosal blood flow, and on ethanol-induced glandular mucosal damage in rats that were fasted for 24 hr before experimentation. The animals were anesthetized with sodium pentobarbitone (50 mg/kg intraperitoneal) and their tracheae cannulated. An ex vivo stomach chamber then was prepared. The luminal bathing solution was collected every 15 min and the concentrations of H+ and Na+ were determined by a pH autotitrator and an ionmeter, respectively. The glandular mucosal blood flow was measured by a laser Doppler flowmeter and the severity of lesions was determined by measuring the hemorrhagic areas. Adenosine administration (2.5 or 7.5 mg/kg, subcutaneous) markedly lowered the H+ and Na+ output but increased the secretory volume and mucosal blood flow in a dose-dependent manner. The same doses of the nucleoside also prevented ethanol-induced mucosal damage. These effects were prevented by pretreatment with theophylline (30 or 60 mg/kg, subcutaneous). Ethanol given alone significantly depressed the H+ and Na+ secretion. Both effects were not modified by adenosine treatment. However, the depressive action of ethanol on mucosal blood flow was prevented by adenosine. These findings indicate that adenosine modulates the physiological function of the stomach. It also directly activates the defensive mechanism of the stomach, which is partially mediated by the improvement of the gastric mucosal blood flow and an increase in the nonacid component of gastric secretion.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 35 (1990), S. 106-112 
    ISSN: 1573-2568
    Keywords: nicotine ; ethanol ; gastric secretion ; gastric lesions ; gastric mucosal blood flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The influences of acute or chronic nicotine pretreatment on ethanol-induced changes on gastric secretion, mucosal blood flow (GMBF), and glandular mucosal damage were studied in anesthetized rats. Ethanol administration decreased gastric acid secretion and GMBF, which were accompanied by a marked increase in gastric mucosal damage. Acute nicotine incubation 2 or 4 mg dose-dependently elevated both the titratable acid in the luminal solution and the gastric secretory volume; it also prevented the depressive action on GMBF and gastric mucosal damage in ethanol-treated animals. Chronic nicotine treatment for 10 days reduced the inhibitory action of ethanol on gastric acid secretion; the higher dose (25 μg/ml drinking water) potentiated the decrease of GMBF and the ulcerogenic property of ethanol. However, chronic treatment with the lower dose (5 μg/ml drinking water) had the opposite effects; it also markedly increased the gastric secretory volume. It is concluded that acute nicotine pretreatment elevates, whereas chronic nicotine pretreatment differentially affects GMBF. These effects could account for their protective or preventive actions on ethanol ulceration. The increase in nonacid gastric secretory volume by nicotine could partially explain its antiulcer effect. Furthermore, the acid secretory state of the stomach appears unrelated to the ulcerogenic property of ethanol.
    Type of Medium: Electronic Resource
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