Effects of pentoxifylline on oxidative stress in rats with abdominal compartment syndrome model
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Background: Abdominal compartment syndrome (ACS) causes severe pathology in the cardiovascular, renal and pulmonary systems. Recent studies showed that pentoxifylline (PTX) has effects on increasing tissue oxygenation, healing capillary refill and reducing superoxides and hydroxyl radicals by inhibiting xanthine oxidase. In this study, our aim was to study the effects of PTX on free oxygen radicals and oxidative damage in rats with ACS model. Materials and methods: ACS model was created in 32 male Wistar-Albino-rats, which were randomized into one of the four study groups: Group A (n: 8), having ACS; Group B (n: 8), having ACS and receiving PTX (50 mg/kg/day) intraperitoneal for 10 days; Group C (n: 8), receiving PTX (50 mg/kg/day) intraperitoneal for 10 days without having ACS; Group D (n: 8), having no ACS and not receiving PTX. On the 11th day blood samples were collected to measure alanine-amino-acid-transferase (ALT) and aspartate-amino-acid-transferase (AST) in the heart, malondialdehyde (MDA), myeloperoxidase (MPO) and glutathione (GSH) in the liver, lung and small bowel. Histopathologic injury scoring was done. Results: Groups were compared in pairs. Group A compared to Group B: ALT increase, liver MDA, lung GSH and MPO decrease were statistically meaningful in Group B. Group A compared to Group C: ALT and liver MPO decrease and liver MDA increase were statistically meaningful in Group A. Group B compared to Group C: ALT increase, MDA and GSH decrease in the lung were statistically meaningful in Group B. Group B compared to Group D: ALT and MPO increase in the small bowel and MPO decrease in the lung were statistically meaningful in Group B. Group A had the highest histopathologic injury scoring. Conclusion: Histopathologically confirmed pentoxifylline was effective in the treatment of ACS in these rat models. (c) 2016 The Authors. Published by Elsevier Ltd on behalf of Surgical Associates Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).










