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  • 1
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    Torino : Periodicals Archive Online (PAO)
    Giornale storico della letteratura italiana. 44 (1904) 104 
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  • 2
    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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  • 3
    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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