Inflammatory oedema induced by Lachesis muta muta (Surucucu) venom and LmTX-I in the rat paw and dorsal skin.

The ability of crude venom and a basic phospholipase A(2) (LmTX-I) from Lachesis muta muta venom to increase the microvascular permeability in rat paw and skin was investigated. Crude venom or LmTX-I were injected subplantarly or intradermally and rat paw oedema and dorsal skin plasma extravasation were measured. Histamine release from rat peritoneal mast cell was also assessed. Crude venom or LmTX-I induced dose-dependent rat paw oedema and dorsal skin plasma extravasation. Venom-induced plasma extravasation was inhibited by the histamine H(1) antagonist mepyramine (6mg/kg), histamine/5-hydroxytriptamine antagonist cyproheptadine (2mg/kg), cyclooxygenase inhibitor indomethacin (5mg/kg), nitric oxide synthesis inhibitor l-NAME (100nmol/site), tachykinin NK(1) antagonist SR140333 (1nmol/site) and bradykinin B(2) receptor antagonist Icatibant (0.6mg/kg). Platelet-activating factor (PAF) antagonist PCA4248 (5mg/kg) had no effect. LmTX-I-induced skin extravasation was inhibited by cyproheptadine, mepyramine, indomethacin and PCA4248, while l-NAME and SR140333 had no effect. Additionally, both Lachesis muta muta venom and LmTX-I concentration-dependently induced histamine release from rat mast cells. In conclusion, Lachesis muta muta venom and LmTX-I increase microvascular permeability by mechanisms involving in vivo mast cell activation and arachidonic acid metabolites. Additionally, crude venom-induced responses also involve substance P, nitric oxide and bradykinin release, whether LmTX-I-induced responses involve PAF.