, 2007) The second phase is also associated with the development

, 2007). The second phase is also associated with the development of an inflammatory response triggered by many mediators such as IL-1β, IL-6, IL-8 and TNF-α ( Chichorro et al., 2004), eicosanoids and NO ( Hunskaar and Hole, 1987; Moore et al., 1991), which prolongs the pain for the measurement remainder time ( Shin et al., 2011). At the doses tested (5, 10 and 20 μg venom/paw), the venom did not produce a significantly effect on nociception test. Although inflammatory Palbociclib order responses have been observed in the paw edema test, it is worth speculating that the venom in larger doses (>20 μg venom/paw) could induce painful response. In fact, 20 μg venom/paw was able to

induce hind-paw edema after 10 min of administration. Phoneutria nigriventer ( Costa et al., 2001; Zanchet and Cury, 2003) and Loxosceles gaucho ( Barbaro et al., 2010) venoms and peptides Nutlin-3a datasheet isolated from Scaptocosa raptoria venom ( Ferreira et al., 1998) also produced edema in rodents. These studies showed that pain and swelling caused by these spider venoms are related, as they involve the same molecular cascades. The cardiotoxic activity of A. paulensis venom and its two chromatographic fractions, LMMF and PF, was evaluated by two assays: in situ frog heart and frog heart ventricular slices.

In both, the venom induced cardiac arrest inhibited by atropine, suggesting the dependence of acetylcholine receptor activation. Only the LMMF was able to produce similar response, indicating the venom peptides are not responsible for it. The venom of the tarantula spider Lasiodora sp. caused a dose-dependent bradycardia, a transient cardiac arrest and rhythm disturbances on isolated rat heart, effects that were enhanced by anticholinesterase drugs, abolished by atropine, inhibited by an inhibitor of ACh vesicular transport, and not

modified by TTX, leading the suggestion that this venom induces see more the release of ACh from parasympathetic nerve terminals by activating TTX-resistant Na+-channels ( Kalapothakis et al., 2003). The dialyzed P. nigriventer venom produced positive inotropic and chronotropic effects in isolated rat heart that were inhibited by β-adrenergic antagonists and potentiated by atropine ( Costa et al., 1998). In a previous study, P. nigriventer whole venom induced negative chronotropic and inotropic effects on isolated guinea pig atria, these effects being abolished by atropine ( Vital-Brazil et al., 1988). While the sympathetic effect is explained by the presence of venom neurotoxins able to modulate Na+-channel activity, the parasympathetic response is probably mediated by the presence of biogenic amines in the venom, which were excluded by venom dialysis ( Costa et al., 1998). In the present study, it was shown that the parasympathetic-like response produced by A. paulensis venom is also due to low molecular mass compounds, possibly biogenic amines also or polyamines.

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