The ability of Bothrops asper snake venom to cause hyperalgesia was investi
gated in rats, using the paw pressure test. Intraplantar injection of the v
enom (5-15 mug/paw) caused a dose and time-related hyperalgesia. which peak
ed 2 h after venom injection. Bothrops asper venom-induced hyperalgesia was
blocked by the bradykinin B-2 receptor antagonist HOE 140 and attenuated b
y dexamethasone, an inhibitor of phospholipase A(2). Inhibition of the lipo
xygenase pathway by NDGA abrogated the algogenic phenomenon. The hyperalges
ic response was not modified by pretreatment with indomethacin, an inhibito
r of the cyclo-oxygenase pathway, by meloxicam, an inhibitor of the type 2
cyclo-oxygenase pathway, by the PAF receptor antagonist BN52021 or by anti-
TNF-alpha or anti-interleukin 1 antibodies. Intraplantar injection of the v
enom also caused an oedematogenic response which was not modified by any of
these pharmacological treatments. These results suggest that hyperalgesia
induced by Bothrops asper venom is, at least partially, mediated by bradyki
nin, phospholipase A(2) activity and leukotrienes. Distinct mechanisms: are
involved in the development of hyperalgesia and oedema induced by the veno
m. (C) 2001 Elsevier Science Ltd. All rights reserved.