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  • 1
    ISSN: 1420-908X
    Keywords: Adaptive cytoprotection ; Lesions ; Nonprotein sulfhydryl compounds
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The contribution of the endogenous nonprotein sulfhydryl compounds (SH) in gastric adaptive cytoprotection was investigated in rats. N-ethylmaleimide (NEM) treatment significantly reduced mucosal SH level, and aggravated the mucosal injury induced by absolute ethanol. Oral administration of the mild irritants, 20% ethanol, 5% NaCl or 0.3 M HCl, significantly increased the basal mucosal SH level. These agents also showed a cytoprotective action against the necrotizing effect of absolute ethanol. Administration of NEM did not alleviate this cytoprotective potential, although it abolished the increased SH level evoked by these mild irritants. Thus, it is concluded that modulation of endogenous SH by mild irritants perhaps only plays a minor role in the gastric adaptive cytoprotection.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 42 (1994), S. 146-148 
    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
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