We have investigated the mechanisms involved in the genesis of edema and nociception induced by the Philodryas patagoniensis venom (PpV) injected into mice footpad. The PpV induced dose-related edema and nociceptive effects. Pre-treatment of mice with cyclooxygenase inhibitor (indomethacin), but not with cyclooxygenase 2 inhibitor (celecoxib) markedly inhibited both effects. Pre-treatments with H1 receptor antagonist (promethazine) or with dual histamine-serotonin inhibitor (cyproheptadine) failed in inhibiting both effects. In groups pre-treated with captopril (angiotensin-converting enzyme inhibitor) the edema was unaltered, but nociception was clearly increased, suggesting the participation of kinins in the pathophysiology of the nociception but not of the edema-forming effect of PpV. When PpV was treated with EDTA, the nociception was similar to the one induced by untreated venom, but edema was markedly reduced. We concluded that PpV-induced edema and nociception have cyclooxygenase eicosanoids as main mediators and no participation of vasoactive amines. Kinins seem to participate in nociception but not in edema induced by PpV. Results also suggest that metalloproteinases are the main compounds responsible for the edema, but not for the nociception induced by this venom.
- The American Society for Pharmacology and Experimental Therapeutics