Pharmacological Profile of Rat Pleurisy Induced by Bothrops jararaca Venom

Abstract

Abstract Bothrops jararaca venom (30 μg/site) triggered a marked inflammatory reaction in the pleural cavity that was long-lasting and reproducible. In the first 1 h after pleurisy induction, a significant decrease of total and differential cell count was observed in comparison with control values, despite the gradual enhancement of fluid leakage. A significant increase of cell migration was observed after 3 h of pleurisy induction, due to mononuclear and neutrophil cells that peaked 8 h later and this was followed by a gradual decrease, remaining elevated up to 24 h. In parallel with cell influx, a significant increase of fluid leakage that peaked between 1 and 8 h was observed, being completely abolished after 12 h following pleurisy induction. This inflammatory response was not associated in parallel with significant changes in circulating leucocyte cells and it was significantly inhibited by compound 48/80, cyproheptadine, pyrilamine, dexamethasone, indomethacin and phenidone. Preheating of the venom (100C) caused a significant decrease of both leakage of fluid and cell migration in the pleural cavity 8 h after pleurisy induction. Previous exposure to the venom (30 μg/site, 5 days before) produced a significant decrease of both cell migration and fluid leakage 4 h after triggering pleurisy with the same dose of the venom. Otherwise, prior daily treatment with the venom (10 μg/site, 4 days) resulted only in marked fluid leakage reduction 1 h after treating the animals with BJV (30 μg/site). These results show that the venom elicits pro-inflammatory effects in the rat pleural cavity which involve the participation of several mediators, including histamine, 5−hydroxytryptamine and products of arachidonic pathways.