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  • 1
    ISSN: 1573-2568
    Keywords: prostaglandin ; duodenal alkaline secretion ; acid-induced duodenal injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the anesthetized rat, exogenous acid (0.1–0.3 N HCl) perfused through the duodenum produced a dose-related increase in the severity of duodenal villous injury. Increasing the duration of perfusion of the 0.1 N HCl also increased the severity of the injury. The increase in the severity of the lesion score was due to an increase in the percentage of villi with damage extending to the lower half of the villus. 16,16-Dimethyl prostaglandin E2 (dm PGE2, 5 μg/kg) administered subcutaneously significantly increased duodenal mucosal alkaline secretion and significantly reduced the duodenal villous injury produced by 0.1 N HCl. The reduction in the severity of the lesion score was due to a decrease in the percentage of villi with the deeper type of damage. These data indicate: (1) perfusion of the rat duodenum with 0.1 N HCl at 0.1 ml/min for 30 min provides a valid model for assessing deep duodenal villous injury, (2) exogenous prostaglandin enhances the resistance of the duodenal mucosa against acid induced deep villous injury, and (3) the enhanced resistance may be mediated at least in part by stimulation of duodenal alkaline secretion. The results support the hypothesis that stimulated duodenal alkaline secretion may play a role in defense of the duodenal mucosa against acid-induced deep villous injury.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 33 (1988), S. 1403-1408 
    ISSN: 1573-2568
    Keywords: ethanol gastric injury ; antral injury ; prostaglandin ; meciadanol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The purpose of this study was to systematically assess 100% ethanol-induced gross and histologic injury of the antral and the corpus mucosa of the rat stomach and the effect of two protective agents, a prostaglandin analog and meciadanol (a flavenoid) on this injury. The gross antral injury was much more subtle than the corpus injury. Therefore, different scoring criteria were developed for the antrum. Surprisingly, however, the extent and severity of histologic injury was similar in both areas. Pretreatment with either meciadanol or 16, 16-dimethyl prostaglandin E2 significantly protected against this injury in the antrum as well as in the corpus.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-2568
    Keywords: ANGIOTENSINOGEN ; ANGIOTENSIN CONVERTING-ENZYME INHIBITOR ; GASTRIC HYPEREMIA ; GROWTH FACTOR
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To assess the mechanism of the effect ofcigarette smoke on ulcer disease we employed a rat modelin which cigarette smoke increases the size of aceticacid-induced gastric ulcer and decreases the hyperemia at the ulcer margin. We postulate thatcigarette smoke increases angiotensin II (avasoconstrictor) in ulcer tissue. Since directmeasurement of angiotensin II in small tissue samples isproblematic, we compared the messenger ribonucleic acid (mRNA)for its precursors (angiotensinogen and renin) in ulcerand normal gastric tissue. We also evaluated the effectof enalapril, which blocks the conversion of angiotensin I to angiotensin II on ulcer size.In the ulcer tissue, cigarette smoke produced asignificant increase in mRNA for angiotensinogen but notfor renin. Enalapril decreased the size of the gastric ulcer in rats exposed to cigarette smoke. Thedata support the possibility that in ulcer tissuecigarette smoke stimulates an angiotensin II-mediatedmechanism, which may in part be responsible for the impairment of ulcer margin hyperemia andaggravation of ulcer size.
    Type of Medium: Electronic Resource
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