Abstract

Background and aims: Although many studies have been made to define the pathophysiology of acute gastric mucosal lesion, its pathogenesis is still not clearly defined. The ischemia of gastric mucosa and decrease in mucus secretion are considered the main causes of acute gastric lesions. It has been shown that antithrombin III (ATIII) inhibits neutrophil infiltration in ischemia-reperfusion injury and increases the secretion of PGI2. The aim of this study was to evaluate the effects of ATIII on gastric mucosal lesions in burned rats. Materials and methods: Thirty Sprague- Dawley male rats were used. They were divided into three groups. A sham burn group (Group 1, n:10) was exposed to 21 OC water. A burn group (Group 2, n:10) and burn + ATIII group (Group 3, n:10) were exposed to 95 OC water for 10 sec., producing full-thickness burn in 30% of total body surface. Group 3 rats received 250 U/kg ATIII via right jugular vein, 15 minutes before burn injury. One ml 0.9% NaCl was given as placebo in Group 1 and Group 2 rats by the same route. The rats of all three groups were killed 12 hours after burn injury by an overdose anesthetic. The stomachs of all the rats were removed and opened along great curvature. Specimens were first evaluated macroscopically. A pathologist evaluated the hisopathologic specimens blindly. Results: There was no macroscopic or microscopic gastric lesions in Group 1. In Group 2, hyperemia in two rats, and erosion in one rat were found macroscopically. Histopathologic examinations revealed acute gastritis in 5 rats (50%) of Group 2; however, there was no acute gastritis in rats treated with ATIII (Group 3) (p

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