Investigation of pulmonary involvement in inflammatory bowel disease in an experimental model of colitis

BACKGROUND/AIMS: Inflammatory bowel disease (IBD) may also involve various extra-intestinal organs. Clinical studies have found asymptomatic/symptomatic pulmonary involvement in 1% to 6% of patients with IBD. The present study histopathologically investigated pulmonary involvement in an experimental model of colitis in order to demonstrate pulmonary tissue involvement in IBD and to expose potential etiological factors. It also explored the relation between inflammation and tissue concentrations of vascular endothelial growth factor (VEGF) and tumor necrosis factor α (TNF-α). METHODS: The study comprised 24 male Wistar albino rats. The rats were divided into four groups of six rats each. Acute colitis was induced in two separate groups using either the dextran sulphate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS) method, while the other two groups were used as controls for each model of colitis. Wallace scoring was used for macroscopic assessment of colitis, and the lungs were histopathologically examined. Concentrations of VEGF and TNF-α in pulmonary tissue were measured by the enzyme-linked immunosorbent assay method. RESULTS: The number of animals that had alveolar hemorrhage was significantly higher in the TNBS-induced colitis and DSS-induced colitis groups compared to their own control groups (p = 0.015 and p = 0.015, respectively). VEGF and TNF-α concentrations in pulmonary tissues were significantly increased in both the TNBS colitis and DSS colitis groups compared to their own control groups (p = 0.002 and p = 0.004, respectively; and p = 0.002 and p = 0.002, respectively). CONCLUSIONS: The present study demonstrated that significant and serious histopathological changes directly associated with colitis occur in the lungs in IBD.

effects of allopurinol on rat liver and spleen tissues in a chronic hyperammonemia animal model

To investigate whether hyperammonemia can lead to any structural change in liver and spleen tissues or biochemical changes in blood and if allopurinol [ALLO] has a protective effect in hyperammonemia. This study was conducted between April and May 2006. Thirty-six females Wistar Albino rats were randomly divided into 3 equal groups: Controls, administered with ammonia [NH[3]] and administered with NH[3] + ALLO groups. Ammonium acetate [2.5 mmole/kg/day] was injected to NH[3] group intraperitoneally [IP] for 28 days. The other group received ammonium acetate [2.5 mmole/kg] plus ALLO [50 mg/kg] IP for 28 days. After finishing the study, blood and tissue samples were collected to perform histopathological and biochemical analysis. Liver and spleen tissues were normal in the control group. In NH3 group, liver tissues were minimally vacuolar and granular degenerations and moderate mononuclear cell infiltration. However, there was no histopathological change in NH[3] + ALLO group. Spleen tissues were normal in NH3 group. In biochemical analysis, there was no significant difference between the groups [p>0.05]. The ammonium acetate may cause minimal structural changes in rat liver and ALLO can prevent this. We found that biochemical parameters do not necessarily correlate with the histopathological findings