RESUMO
Background: Tramadol is centrally acting analgesic that is frequently used clinically but its mechanism of action is still unclear
Aim of work: To evaluate tramadol analgesic activity, and its effect on gastric mucosa and hormones
Material and Methods: Thirty two adult male albino rats were used. Rats were divided into three groups: group [I] was injected with 3 doses of physiological saline [2ml kg[-1] every 12 h, i.p.], served as control; group [II] was injected with 3 doses of indomethacin [10 mg kg[-1] every 12 h, i.p.]; and group [III] was injected with 3 doses of tramadol [10 m kg[-1] every 12 h, i.p.]. 30 min after the first dose of injections, all groups were given 10 ml k[-1] of 1% acetic acid-saline i.p. to induce writhing. After 10 min following acetic acid injection, writhes numbers were counted over 20 min. Gastric mucosa was examined macroscopically and microscopically. Gastrin expression was detected by immunohistochemistry. Serum prostaglandin [PG], E2, ghrelin, and histamine concentrations were measured using ELISA kits
Results: Tramadol has lower analgesic effect compared to indomethacin. The gastric ulcer index was significantly lower in tramadol- versus indomethacin-treated group [P <0.0001]. Immunohistochemistry demonstrated higher gastrin immunoreactivity in indomethacin- and tramadol-treated groups versus control. Ghrelin serum levels were significantly suppressed by tramadol and indomethacin versus control that were coincident with gastric mucosal lesions. No significant changes in serum levels of PGE2 and histamine were obtained
Conclusion: Our results suggested that tramadol-induced gastric lesions are probably mediated by reduction of ghrelin and increase in gastrin expression. The antinociceptive and gastric effects of tramadol suggest that tramadol is relatively safe clinically in pain therapy