Akademik Veri Yönetim Sistemi
DISEASES OF THE ESOPHAGUS, cilt.28, sa.3, ss.253-257, 2015 (SCI-Expanded)
Esophageal stricture, one of the important complications of corrosive esophagus, develops following edema and granulation tissue that forms during and after the inflammatory reactions. Tenoxicam, a non-steroid anti-inflammatory drug with a long half-life, prevents various leukocyte functions including phagocyte and histamine secretion by inhibiting prostaglandin synthesis and removes various oxygen radicals in the region of inflammation. We designed this as a histopathological study using tenoxicam in rats for which we created a corrosive esophagus model. After necessary authorizations were obtained, the study was performed in Canakkale 18 Mart University experimental animal laboratory. Twenty-four Wistar albino rats, weighing 220-240g, were used for the experiment. Experimental animals were randomized into three groups: tenoxicam group (group T, n:8), control group (group C, n:8), and sham group (group S, n:8). Tenoxicam 0.5mg/kg/day was administered to animals in group T, where esophageal burn was developed experimentally, 5mg/kg 0.9% NaCL was administered i.p. to rats in group C for 15 days, once in 24 hours. No procedure was applied to rats in group S. After 15 days, all animals were sacrificed under general anesthesia and their esophagi were extracted. As a result of histopathological evaluation, inflammation and fibroblast proliferation was not observed in rats in the sham group (group S). Intense inflammation was observed in six rats (6+/2-) in the control group, and fibroblast proliferation was observed as 5+/3-. And in treatment groups, inflammation was evaluated as 3+/5-, and fibroblast proliferation as 3+/5-. In our study, histopathologic damage score was higher in the control group (P < 0.005). We deduce that tenoxicam can be useful in the treatment of caustic esophageal injuries in the acute phase, but think that these drugs require further researches and clinical studies before routine clinical use.