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Pharmacological Characterization Of The Edema Caused By Vitalius Dubius (theraphosidae, Mygalomorphae) Spider Venom In Rats
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Pharmacological Characterization Of The Edema Caused By Vitalius Dubius (theraphosidae, Mygalomorphae) Spider Venom In Rats. Amer Soc Pharmacology Experimental Therapeutics, v. 356, p. 13-19 JAN-2016.
0022-3565
WOS:000366942000003
10.1124/jpet.115.226787
Autor
Rocha-e-Silva
Thomaz A. A.; Linardi
Alessandra; Antunes
Edson; Hyslop
Stephen
Institución
Resumen
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Bites by tarantulas (Theraphosidae, Mygalomorphae) in humans can result in mild clinical manifestations such as local pain, erythema, and edema. Vitalius dubius is a medium-sized, non-aggressive theraphosid found in southeastern Brazil. In this work, we investigated the mediators involved in the plasma extravasation caused by V. dubius venom in rats. The venom caused dose-dependent (0.1-100 mu g/site) edema in rat dorsal skin. This edema was significantly inhibited by ((S) 1-{2-[3(3-4-dichlorophenyl)- 1-(3-iso-propoxyphenylacetyl) piperidine-3-yl] ethyl}-4-phenyl-1-azoniabicyclo[2.2.2] octone, chloride) (SR140333, a neurokinin NK1 receptor antagonist), indomethacin [a nonselective cyclooxygenase (COX) inhibitor], cyproheptadine (a serotonin 5-hydroxytryptamine(1/2) and histamine H-1 receptor antagonist), and N-omega-nitro-L-arginine methyl ester (a nitric oxide synthase inhibitor). In contrast, mepyramine (a histamine H-1 receptor antagonist), D-Arg-[Hyp(3), Thi(5), D-Tic(7), Oic(8)-]-BK (JE 049, a bradykinin B-2 receptor antagonist), and ((S)-N-methyl-N-[4-(4-acetylamino-4-phenylpiperidino)-2-(3,4-di-chlorophenyl)butyl] benzamide) (SR48968, a neurokinin NK2 receptor antagonist) had no effect on the venom-induced increase in vascular permeability. In rat hind paws, the venom-induced edema was attenuated by ketoprofen (a nonselective COX inhibitor) administered 15 minutes postvenom. Preincubation of venom with commercial antiarachnid antivenom attenuated the venom-induced edema. These results suggest that the enhanced vascular permeability evoked by V. dubius venom involves serotonin, COX products, neurokinin NK1 receptors, and nitric oxide formation. The attenuation of hind paw edema by ketoprofen suggests that COX inhibitors could be useful in treating the local inflammatory response to bites by these spiders. 356 1
13 19 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Research Support Fund of the Faculdade de Ciencias Medicas da Santa Casa de Sao Paulo [FAP-FCMSCSP] Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)