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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 202 (1994), S. 947-953 
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 45 (1989), S. 734-736 
    ISSN: 1420-9071
    Keywords: Gastrin release ; rat isolated stomach ; baclofen ; GABA-A receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary In order to investigate the role of peripheral GABA-B receptors, the effects of the putative GABA-B agonist baclofen on immunoreactive gastrin release from an isolated vascularly perfused rat stomach preparation were examined. The vascular infusion of baclofen at graded concentrations induced a dose-dependent increase in gastrin release; this was unaffected by the GABA-B antagonist delta-aminovaleric acid, but was fully prevented by the selective GABA-A antagonist bicuculline as well as by atropine or tetrodotoxin. These results suggest that the stimulant effects of baclofen are mediated by nervous cholinergic structures, associated with GABA-A receptors, and indicate that this GABA-B agonist must be regarded as a partial agonist of peripheral GABA-A receptors.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The antiinflammatory activity of a new 14-membered macrolide antibiotic, roxithromycin, was evaluated in various rat models including carrageenan- and poly-l-arginine-induced hind-paw oedema, croton oil inflamed ear assay and polyester sponge granuloma. When administered orally to animals, roxithromycin displayed an atypical profile in the assays utilized, including: (1) marked antioedema activity similar to that of indomethacin in poly-l-arginine assay, (2) significant inhibition of λ-carrageenan hind-paw oedema and croton-oil-induced inflammation in the ear, although indomethacin was more effective, and (3) failure to reduce the development of granuloma induced by implanted polyester sponges, while indomethacin significantly reduced the chronic inflammatory reaction. Based on these results, it is concluded that roxithromycin is active in reducing the acute inflammatory reaction in rat models through mechanisms different from conventional nonsteroidal antiinflammatory agents such as indomethacin. Therefore, roxithromycin may have a favorable impact on skin inflammatory reactions accompanying microbial infections.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 39 (1994), S. 2109-2117 
    ISSN: 1573-2568
    Keywords: omeprazole ; hemorrhagic shock ; gastric damage ; gastroprotection ; mucus secretion ; acid output
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The efficacy of omeprazole in preventing gastric mucosal injury induced by hemorrhagic shock in rats and the putative mechanisms involved in this effect were investigated in the present study. Omeprazole did not affect mean arterial blood pressure under both basal conditions and induction of hemorrhagic shock, but it evoked a marked increase in Alcian blue recovery from gastric preepithelial mucus. The morphometric analysis of histological sections revealed that omeprazole caused a significant reduction of hemorrhagic shock-induced damage of gastric mucosa. Ranitidine, used as the reference drug, failed to affect mean arterial blood pressure, Alcian blue recovery from gastric mucus, or hemorrhagic shock-induced damage of gastric mucosa. Both omeprazole and ranitidine exerted a significant inhibition of gastric acid output from anesthetized pylorus-ligated rats. Overall, the present results indicate that omeprazole is effective in protecting gastric mucosa from necrotic damage induced by hemorrhagic shock and suggest that an enhancement of gastric mucus secretion contributes to this protective action.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1573-2568
    Keywords: SURAMIN ; ETHANOL ; GASTRIC DAMAGE ; GASTROPROTECTION ; MUCUS SECRETION ; ACID SECRETION
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Suramin is currently used in clinical practiceas antineoplastic agent because of its complexinteraction with the biological activity of variousgrowth factors involved in tumor progression. Theinfluence exerted by suramin on gastric injury induced inrats by intraluminal injection of absolute ethanol wasinvestigated in the present study. The morphometricanalysis of gastric histological sections revealed that suramin, 18 mg/kg, administeredintraperitoneally for 14 days every other day, caused amarked enhancement of ethanol-induced mucosal damage.This effect was more pronounced 1-8 hr following ethanol administration, and it was still significantafter 48 hr. In suramin-treated animals the evaluationof Alcian blue recovery from gastric-bound mucus showedthat the levels of adherent mucus were significantly lower than those detected in untreated rats. Inaddition, pretreatment with suramin did not modify basalacid secretion, but caused potentiation of acid outputstimulated by pylorus ligation or electrical vagal stimulation. Overall, the present resultsindicate that suramin exerts a negative influence onboth gastric protective and repairing mechanisms. Due tothe peculiar pharmacodynamic profile of suramin, it is suggested that interference withendogenous growth factors, endowed with physiologicalprotective activity on gastric mucosa, might account forthe damage-enhancing action of this drug.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1573-2568
    Keywords: LANSOPRAZOLE ; GASTRIC DAMAGE ; GASTROPROTECTION ; MUCUS SECRETION
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The protective effects of the proton pumpinhibitor lansoprazole on gastric mucosal damage inducedby ethanol-HCl or hemorrhagic shock were investigated inthe present study. The morphometric analysis of gastric histological sections revealed thatlansoprazole dosedependently reduced mucosal injuryevoked by ethanol-HCl (ED50 = 24.3μmol/kg) or hemorrhagic shock (ED50 = 38.9μmol/kg), these effects being associated with markedincrements of Alcian blue recovery from gastric boundmucus (ED50 = 31.4 μmol/kg and 27.6μmol/kg, respectively). In addition, lansoprazoleinhibited gastric acid secretion from pylorusligated rats(ED50 = 9.8 μmol/kg). Further experiments,performed on rats with ethanol-HCl-induced gastricinjury, indicated that the protective effects of lansoprazole were not modified by L-365,260,suramin, NG-nitro-L-arginine, or systemicablation of capsaicin-sensitive sensory nerves, whereasthey were partly blocked by indomethacin and fullyprevented by N-ethyl-maleimide. In addition, lansoprazoledid not modify somatostatin concentrations in gastricmucosa. The present results provide evidence thatlansoprazole prevents the necrotic damage of gastric mucosa induced by ethanol-HCl or hemorrhagicshock. According to the rank order of ED50values, these effects appear to depend mainly on theenhancement of the gastric mucus barrier rather than on the reduction of acid secretion. It is alsoproposed that an increased production of prostaglandins,as well as an increased availability of sulfhydrylcompounds at level of gastric mucosa may account for the gastroprotective effects oflansoprazole.
    Type of Medium: Electronic Resource
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