dc.creatorFerreira, Tatiane
dc.creatorCamargo, Enilton A
dc.creatorRibela, Maria Teresa C P
dc.creatorDamico, Daniela C
dc.creatorMarangoni, Sérgio
dc.creatorAntunes, Edson
dc.creatorDe Nucci, Gilberto
dc.creatorLanducci, Elen C T
dc.date2009-Jan
dc.date2015-11-27T13:15:27Z
dc.date2015-11-27T13:15:27Z
dc.date.accessioned2018-03-29T01:09:15Z
dc.date.available2018-03-29T01:09:15Z
dc.identifierToxicon : Official Journal Of The International Society On Toxinology. v. 53, n. 1, p. 69-77, 2009-Jan.
dc.identifier0041-0101
dc.identifier10.1016/j.toxicon.2008.10.016
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/18996140
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/198424
dc.identifier18996140
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1298657
dc.descriptionThe 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.
dc.description53
dc.description69-77
dc.languageeng
dc.relationToxicon : Official Journal Of The International Society On Toxinology
dc.relationToxicon
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subjectAnimals
dc.subjectCell Movement
dc.subjectCrotalid Venoms
dc.subjectEdema
dc.subjectFoot
dc.subjectInflammation
dc.subjectMast Cells
dc.subjectNitric Oxide
dc.subjectProstaglandin-endoperoxide Synthases
dc.subjectRats
dc.subjectReceptor, Bradykinin B2
dc.subjectReceptors, Tachykinin
dc.subjectSkin
dc.subjectViperidae
dc.titleInflammatory Oedema Induced By Lachesis Muta Muta (surucucu) Venom And Lmtx-i In The Rat Paw And Dorsal Skin.
dc.typeArtículos de revistas


Este ítem pertenece a la siguiente institución