INTRODUCTION: An experimental study was conducted to investigate the effects of erythropoietin on the acute phase of esophageal burn damage induced by sodium hydroxide. MATERIALS AND METHODS: A standard esophageal alkaline burn was produced by the application of 10% sodium hydroxide to the distal esophagus in an in vivo rat model. Fifty-six female rats were allocated into three groups: Group BC (baseline control, n = 8) rats were uninjured and untreated, Group PC (positive control, n = 24) rats were injured but untreated and Group EPO (erythropoietin-treated, n = 24) rats were injured and given subcutaneous erythropoietin (1,000 IU/kg per day), 15 min, 24, and 48 h after administration of the NaOH solution. Six animals from Group PC and six from Group EPO were killed at 4, 24, 48, and 72 h after application of NaOH to the esophagus. All of animals in Group BC were killed 4 h after exposure to 0.9% NaCl. Oxidative damage was assessed by measuring levels of malondialdehyde (MDA) and nitric oxide (NO), and activities of superoxide dismutase (SOD) and catalase (CAT) in homogenized samples of esophageal tissue. Histologic damage to esophageal tissue was scored by a single pathologist blind to groups. RESULTS: MDA levels in the BC and EPO groups were significantly lower than those in the PC group (p < 0.05). CAT and SOD activities, and NO levels in the BC and EPO groups were significantly higher than in the PC group (p < 0.05). Esophageal tissue damage measured at 4, 24, 48, and 72 h after NaOH application was significantly less in the EPO group than in the PC group (p < 0.05). CONCLUSIONS: When administered early after an esophageal burn induced by 10% sodium hydroxide in this rat model, erythropoietin significantly attenuated oxidative damage, as measured by biochemical markers and histologic scoring.
INTRODUCTION: An experimental study was conducted to investigate the effects of erythropoietin on the acute phase of esophageal burn damage induced by sodium hydroxide. MATERIALS AND METHODS: A standard esophageal alkaline burn was produced by the application of 10% sodium hydroxide to the distal esophagus in an in vivo rat model. Fifty-six female rats were allocated into three groups: Group BC (baseline control, n = 8) rats were uninjured and untreated, Group PC (positive control, n = 24) rats were injured but untreated and Group EPO (erythropoietin-treated, n = 24) rats were injured and given subcutaneous erythropoietin (1,000 IU/kg per day), 15 min, 24, and 48 h after administration of the NaOH solution. Six animals from Group PC and six from Group EPO were killed at 4, 24, 48, and 72 h after application of NaOH to the esophagus. All of animals in Group BC were killed 4 h after exposure to 0.9% NaCl. Oxidative damage was assessed by measuring levels of malondialdehyde (MDA) and nitric oxide (NO), and activities of superoxide dismutase (SOD) and catalase (CAT) in homogenized samples of esophageal tissue. Histologic damage to esophageal tissue was scored by a single pathologist blind to groups. RESULTS: MDA levels in the BC and EPO groups were significantly lower than those in the PC group (p < 0.05). CAT and SOD activities, and NO levels in the BC and EPO groups were significantly higher than in the PC group (p < 0.05). Esophageal tissue damage measured at 4, 24, 48, and 72 h after NaOH application was significantly less in the EPO group than in the PC group (p < 0.05). CONCLUSIONS: When administered early after an esophageal burn induced by 10% sodium hydroxide in this rat model, erythropoietin significantly attenuated oxidative damage, as measured by biochemical markers and histologic scoring.
Authors: M Bingöl-Kologlu; F C Tanyel; S Müftüoğlu; N Renda; N Cakar; N Büyükpamukçu; A Hiçsönmez Journal: J Pediatr Surg Date: 1999-02 Impact factor: 2.545
Authors: Hasan Kahraman; Ergül Kurutaş; Mahmut Tokur; Selim Bozkurt; Harun Cıralık; Betül Kabakcı; Nurhan Köksal; Vedat Balkan Journal: Balkan Med J Date: 2013-03-01 Impact factor: 2.021