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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 39 (1994), S. 934-939 
    ISSN: 1573-2568
    Keywords: aspirin ; prostaglandin E1 ; misoprostol ; ulcer healing
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Clinical studies have suggested that treatment with the prostaglandin E1 analog, misoprostol, leads to significant healing of ulcers in patients taking regular nonsteroidal antiinflammatory therapy. This study aimed to investigate mechanisms involved in this healing using a rat model. Gastric ulcers were induced by application of acetic acid using a standard technique. Rats were treated with 200 mg/kg aspirin, 100 µg/kg misoprostol, a combination of both treatments, or methylcellulose vehicle for up to two weeks, starting two days after ulcer induction. Ulcers were assessed by macroscopic measurements of area and by quantitative histological measurements. Aspirin delayed ulcer healing compared with controls, while misoprostol significantly reversed this effect. Quantitative histology revealed that misoprostol cotreatment significantly increased mucosal regeneration compared with aspirin treatment alone. However, misoprostol did not reverse the effects of aspirin on an index of wound contraction. We conclude that treatment with misoprostol significantly reverses the delayed healing effect of aspirin, and this may occur via an effect on epithelial regeneration.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-2568
    Keywords: aspirin ; indomethacin ; gastric ulcer ; ulcer healing ; cell proliferation ; regeneration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Nonsteriodal antiinflammatory drugs initiate gastric ulceration and delay gastric ulcer healing. This study aimed to investigate the role of epithelial cell proliferation in delayed ulcer healing and to identify the most reproducible technique for measuring cell proliferation. Rats with acetic acid-induced gastric ulcers were treated for two weeks with indomethacin (1 mg/kg), aspirin (200 mg/kg), or vehicle control. Ulcers were assessed by macroscopic measurement of ulcer area, quantitative histological measurement of mucosal regeneration, and 5-bromo-2′-deoxyuridine immunohistochemistry to assess epithelial cell proliferation. Indomethacin and aspirin significantly delayed ulcer healing and inhibited mucosal regeneration. Three techniques for assessing cell proliferation were compared, and a scoring system, designed to take into account the entire tissue, was shown to be the most reproducible technique. Indomethacin significantly enhanced cell proliferation in the fundic area of ulcer and aspirin had no effect on cell proliferation. We conclude that aspirin and indomethacin delay ulcer healing by an inhibition of mucosal regeneration, but they do not inhibit epithelial cell proliferation.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 41 (1996), S. 1838-1844 
    ISSN: 1573-2568
    Keywords: aging ; gastric ulcer ; ulcer healing ; indomethacin ; acetic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study aimed to investigate the effect of age on natural ulcer healing and delayed ulcer healing induced by nonsteroidal antiinflammatory drugs, using a rat model. Gastric ulcers were induced in young, adult, and aged rats using serosal or mucosal (kissing ulcers) application of acetic acid. Rats were treated with indomethacin 1 mg/kg/day subcutaneously or vehicle for two weeks. Ulcers were assessed by macroscopic and histological measurements of ulcer size. Ulcer induction was affected by age. Aged rats developed significantly smaller ulcers when induced by serosal application of acetic acid and significantly larger ulcers from mucosal application of acetic acid. However, measurements of ulcer size from both models showed no age-related differences in natural ulcer healing. Similarly, indomethacin-induced delayed gastric ulcer healing was not effected by age. We conclude that there are age-related differences in the development of gastric ulcers but there are no age-related differences in natural or delayed ulcer healing in rats.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-2568
    Keywords: GASTRIC MUCOSA ; ISCHEMIA-REPERFUSION ; LEUKOCYTE ; ENDOTHELIUM ; ADHESION
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Leukocyte infiltration is an important step inpostischemic tissue damage. This study aimed todetermine the expression of adhesion molecules and theirrelationship with leukocyte infiltration in thepostischemic gastric mucosa. Gastric tissue was obtainedfrom rats subjected to 30 min gastric ischemia followedby reperfusion. Sections were stained with specificantibodies against (1) L-selectin and (2) LFA-1 on leukocytes, (3) ICAM-1 on endothelial cells,(4) PMNs, and (5) monocytes. Stained cells or bloodvessels in mucosal tissue were counted using imageanalysis. Results showed that from 5 min of reperfusion, numbers of L-selectin-positive cells decreased,whereas LFA-1-positive cells and PMNs increased comparedwith controls. ICAM-1 expression did not increase until60 min of reperfusion. Monocyte numbers were unaffected by reperfusion. We conclude thatgastric ischemiareperfusion results in a rapid influx ofLFA-1-positive cells, the majority of which are PMN.L-Selectin is shed from these cells allowing them to adhere to the microvasculature viaconstitutively expressed ICAM-1.
    Type of Medium: Electronic Resource
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