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  • 1995-1999  (2)
  • ACTIVE OXYGEN METABOLISM  (1)
  • COMPOUND 48/40  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Relationship Between Changes of Active Oxygen Metabolism and Blood Flow and Formation, Progression, and Recovery of Lesions in Gastric Mucosa of Rats with a Single Treatment of Compound 48/80, a Mast Cell Degranulator (1997)
    Springer
    Digestive diseases and sciences 42 (1997), S. 1221-1232 
    Details
    ISSN: 1573-2568
    Keywords: COMPOUND 40/80 ; MAST CELL DEGRANULATOR ; GASTRIC MUCOSA ; MUCOSAL LESION RAT ; ACTIVE OXYGEN METABOLISM ; OXIDATIVE STRESS ; BLOOD FLOW ; ISCHEMIA-REPERFUSION
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The relationship between the changes of activeoxygen metabolism and blood flow and the formation,progression, and recovery of lesions was examined in thegastric mucosa of rats treated once with compound 48/80, a mast cell degranulator. Gastricmucosal lesions appeared 0.5 hr after compound 48/80treatment, became worst at 3 hr, and recovered fairlywell at 12 hr. Increases in gastric mucosal lipidperoxide content and xanthine oxidase andmyeloperoxidase activities and decreases in gastricmucosal vitamin E and hexosamine contents andSe-dependent glutathione peroxidase activity occurredwith the formation and progression of gastric mucosal lesions.These changes were attenuated with the recovery of thelesion. Gastric mucosal nonprotein SH content decreasedwith the formation of gastric mucosal lesions, and this decreased SH content returned to nearthe original level with lesion progression. No changesin gastric mucosal superoxide dismutase and catalaseactivities occurred with the formation, progression, and recovery of gastric mucosal lesions.Gastric mucosal blood flow decreased with the formationof gastric mucosal lesions, and this decreased bloodflow recovered with lesion progression. Serum serotonin concentration, an index of mast celldegranulation, increased with the formation of gastricmucosal lesions, and this increased serotonin level wasattenuated with lesion progression and recovery.Pretreatment with ketotifen, a connective tissue mast cellstabilizer, prevented the formation of gastric mucosallesions, the increases of gastric mucosal lipid peroxidecontent, xanthine oxidase and myeloperoxidase activities, and serum serotonin level; and thedecreases of gastric mucosal nonprotein SH content,glutathione peroxidase activity, and blood flow found at0.5 hr after compound 48/80 treatment. These results indicate that the changes of gastric mucosalactive oxygen metabolism and blood flow are closelyrelated to the formation, progression, and recovery ofgastric mucosal lesions in rats with a single compound 48/80 treatment. The present results alsosuggest that this compound 48/80-induced gastric mucosalinjury could be a kind of ischemia-reperfusion-inducedinjury occurring through degranulation of connective tissue mast cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018854107623
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Participation of Xanthine-Xanthine Oxidase System and Neutrophils in Development of Acute Gastric Mucosal Lesions in Rats with a Single Treatment of Compound 48/80, a Mast Cell Degranulator (1999)
    Springer
    Digestive diseases and sciences 44 (1999), S. 1865-1874 
    Details
    ISSN: 1573-2568
    Keywords: COMPOUND 48/40 ; GASTRIC MUCOSAL LESIONS ; XANTHINE OXIDASE ; NEUTROPHILS ; LIPID PEROXIDE
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The participation of xanthine-xanthine oxidaseand neutrophils in the development of acute gastricmucosal lesions was examined in rats injected once withcompound 48/80, a mast cell degranulator. Gastric mucosal lesions appeared 0.5 hr after compound48/80 injection and developed at 3 hr. The formation ofgastric mucosal lesions at 0.5 hr after compound 48/80injection was prevented by pretreatment with anti-neutrophil antiserum and NPC 14686, anantiinflammatory agent, but not with allopurinol, axanthine oxidase inhibitor. The development of gastricmucosal lesions at 3 hr after compound 48/80 injection was prevented by pretreatment withanti-neutrophil antiserum, NPC 14686, or allopurinol.Increases in the activities of gastric mucosal xanthineoxidase and myeloperoxidase, an index of neutrophilinfiltration, and the content of lipid peroxide occurred 0.5hr after compound 48/80 injection, and these increaseswere enhanced at 3 hr. The increases in gastric mucosalmyeloperoxidase activity and lipid peroxide content at 0.5 hr after compound 48/80injection were attenuated by pretreatment withanti-neutrophil antiserum and NPC 14686, while only theincrease in gastric mucosal xanthine oxidase activity atthe same time point was arrested by allopurinolpretreatment. The increases in gastric mucosal xanthineoxidase and myeloperoxidase activities and lipidperoxide content at 3 hr after compound 48/80 treatment were attenuated by pretreatment withanti-neutrophil antiserum, NPC 14686, or allopurinol.When compound 48/80-injected rats were treated withallopurinol at 0.5 hr after compound 48/80 injection,the progression of gastric mucosal lesions at 3 hr after theinjection was almost completely prevented withinhibition of the increases in gastric mucosal xanthineoxidase and myeloperoxidase activities and lipidperoxide content. These results indicate that in ratswith a single compound 48/80 treatment neutrophilsinfiltrated into the gastric mucosa participated in thedevelopment of acute gastric mucosal lesions and that the xanthine-xanthine oxidase system in thegastric mucosa participated in the progression ratherthan the formation of the gastric mucosallesions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018803025043
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
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