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The effects of tramadol on pathohistological alterations of gastric mucosa in stressed rats.

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The effects of tramadol on pathohistological alterations of gastric mucosa in stressed rats.pdf (8.787Mb)
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2018-09-07
Аутори
Милица, Мијовић
Станојевић, Зорица
Метаподаци
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Апстракт
Introduction and aim: The aim of our research was to examine the effect of tramadol on presence of stress-induced ulcer lesions, as well as pathohistological alterations of gastric mucosa in rats exposed to cold restraint stress (CRS). Material and methods: The experiment was performed on male Wistar rats, weighing 220g, exposed to cold restraint stress (CRS). Animals was pretreated with tramadol (Tramadol®) in the doses of 100mg/kg body weight, injected intraperitoneally, just before cold restraint stress. The total size of lesions was expressed as ulcer index (UI). The pathohistological samples were analyzed by Leica DML S2 light microscope. Results: In animals exposed to CRS there was macroscopically observed deep, dark erosions, and the UI was 4,98±6,18mm 2 . The presence of shallow and deep defects of the mucosa was pathohistological confirmed, but also the presence of extravasated erythrocytes and hyperemic blood vessels. In the submucosa and l.m. mucosae the signs of inflammation were noted, i.e., edema and mass of leucocytes (polymorphonuclears). Tramadol decreased overall surface of the alterations in statistically significant manner, i.e., UL from 4,98 mm 2 to 0,02±0,04 mm 2 (p<0,001). The mucosal defects of the mucosa were observed pathohistological, on the surface itself, but without accompanying bleeding. In the submucosal and l-m. mucosae hyperemia, as well as mass of leucocytes and mastocytes were noted. On the surface of the mucosa, painted with PAS painted mucosa cells and abundant presence of mucosa. Conclusion: Pre-treatment with tramadol can prevent the development of ulcer lesions, and thus if influences gastric pathohistological alterations in stressed rats.
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https://platon.pr.ac.rs/handle/123456789/466
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M34
openAccess
M34
openAccess
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