Objective: was to examine agar as a phlogistic agent in the air pouch model. Method and Materials: Rats were divided into five groups and the effects of 1%, 2%, 3% and 4% agar in the air pouch model were compared with those of 1% carrageenan. The vascular inflammation induced by agar and the microvasculature of the air pouch membrane were analysed. In addition, the role of nitric oxide (NO)-dependent pathways and cellular migration in the responses to 2% agar were evaluated. To assess the mechanism of action underlying the inflammatory effects of agar, rats were treated with a standard anti-inflammatory drug, either celecoxib or acetylsalicylic acid. In addition, a differential leucocyte cell count, total cell count and NO and PGE2 concentrations were determined. Results: The 2% agar was chosen as the optimal concentration. Celecoxib or ASA both inhibited the inflammatory effects of agar, reducing the area of the microvasculature in the tissue lining the air pouch, as well as NO and PGE2 concentrations and cell migration in the exudate. Conclusion: The present study shows that a simple and alternative method (agar) produces consistent results in the air pouch model and can be used as an alternative experimental model of inflammation.
Key words: agar, animal models, inflammation, Wistar rats.