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  • 1
    Electronic Resource
    Electronic Resource
    The gastric cytoprotective action of adenosine and prostaglandin E2 in rabbits (1994)
    Springer
    Inflammation research 42 (1994), S. 146-148 
    Details
    ISSN: 1420-908X
    Keywords: Adenosine ; Prostaglandin E2 ; Gastric gland ; Damage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The direct protective action of adenosine and prostaglandin E2 (PGE2) was examined in an isolated gastric gland preparation in rabbits. Ethanol, (8%, v/v) incubation markedly increased the release of lactate dehydrogenase (LDH) and number of non-viable glands in the preparation. Both effects were prevented by PGE2 preincubation in a concentration (10−6, 1.4×10−5 or 2.8×10−5 M)-dependent manner. The protective action was smaller in adenosine-treated groups, and yet the highest concentration (10−4 M) of the compound also significantly inhibited the cytotoxic effects of ethanol. These findings indicate that both adenosine and PGE2 possess cytoprotective action on gastric glands in rabbits, but the former compound exerts its action beyond physiological concentrations. It is concluded that endogenous PGE2, but not adenosine may act as an ulcer modulator in the stomach.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01983481
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    The influence of acute or chronic nicotine treatment on ethanol-induced gastric mucosal damage in rats (1990)
    Springer
    Digestive diseases and sciences 35 (1990), S. 106-112 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF01537231
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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