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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampFerreira, Heloísa Helena de Araújopt_BR
dc.contributor.authorunicampAntunes, Edsonpt_BR
dc.contributor.authorunicampDe Nucci, Gilbertopt_BR
dc.typeArtigopt_BR
dc.titleInhibition of eosinophil chemotaxis by chronic blockade of nitric oxide biosynthesispt_BR
dc.title.alternativeen
dc.contributor.authorFerreira, H.H.A.pt_BR
dc.contributor.authorLima, C.S.P.pt_BR
dc.contributor.authorMedeiros, M.V.pt_BR
dc.contributor.authorSannomiya, P.pt_BR
dc.contributor.authorFlores, C.A.pt_BR
dc.contributor.authorAntunes, E.pt_BR
dc.contributor.authorDe Nucci, G.pt_BR
dc.subjectÓxido nítricopt_BR
dc.subjectPleurisiapt_BR
dc.subject.otherlanguageNitric oxidept_BR
dc.subject.otherlanguagePleurisypt_BR
dc.description.abstractThe effect of chronic N-omega-nitro-L-arginine methyl ester (L-NAME) treatment on the in vivo eosinophil migration induced by bradykinin, platelet-activating factor (PAF), lipopolysaccharide and carrageenin has been investigated in the rat using the pleurisy model, The in vitro (microchemotaxis chamber) eosinophil migration induced by N-formyl-methionyl-leucyl-phenylalanine (fMLP), PAF and zymosan-activated serum was also evaluated in the rat. The eosinophils were obtained from the peritoneal cavity of male Wistar rats and isolated on a discontinuous metrizamide gradient. Chronic inhibition of nitric oxide biosynthesis was achieved by adding L-NAME to the drinking water to give an intake of approximately 75 mu mol/rat/day for 4 weeks. Rats treated chronically with L-NAME developed a significant level of hypertension (163 +/- 4.8 mmHg; P < 0.01) compared with animals which received either the same dose of the inactive enantiomer D-NAME (124 +/- 3.2 mmHg) or tap water alone (119 +/- 1.6 mmHg). The intrapleural injection of bradykinin (50 mu g), PAF (1 mu g), lipopolysaccharide (0.25 mu g) and carrageenin (125 mu g) into untreated rats in vivo induced a significant level of eosinophil migration by 24 h post-injection. This migration was markedly reduced in L-NAME-treated rats. Eosinophils obtained from untreated rats showed a significant level of migration in vitro in response to fMLP (5 x 10(-8) M), PAF (10(-8) M) and zymosan-activated serum (27 mu l). In contrast, the migration induced by these chemotactic agents was markedly reduced in cells isolated from animals treated chronically with L-NAME. L-Arginine (5.5 mM), but not D-arginine (5.5 mM), restored the ability of eosinophils from L-NAME-treated animals to migrate in response to fMLP. Our results indicate that nitric oxide plays a major role in the in vivo and ex vivo migration of eosinophilspt
dc.relation.ispartofEuropean journal of pharmacologypt_BR
dc.relation.ispartofabbreviationEur. j. pharmacol.pt_BR
dc.publisher.cityAmsterdam pt_BR
dc.publisher.countryPaíses Baixospt_BR
dc.publisherElsevierpt_BR
dc.date.issued1996pt_BR
dc.date.monthofcirculationAug.pt_BR
dc.identifier.citationEuropean Journal Of Pharmacology. Elsevier Science Bv, v. 310, n. 41700, n. 201, n. 207, 1996.pt_BR
dc.language.isoengpt_BR
dc.description.volume310pt_BR
dc.description.issuenumber2-3pt_BR
dc.description.firstpage201pt_BR
dc.description.lastpage207pt_BR
dc.rightsfechadopt_BR
dc.sourceWeb of Sciencept_BR
dc.identifier.issn0014-2999pt_BR
dc.identifier.eissn1879-0712pt_BR
dc.identifier.doi10.1016/0014-2999(96)00379-2pt_BR
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/0014299996003792pt_BR
dc.description.sponsorship1pt_BR
dc.date.available2014-12-02T16:29:41Z
dc.date.available2015-11-26T17:08:47Z-
dc.date.accessioned2014-12-02T16:29:41Z
dc.date.accessioned2015-11-26T17:08:47Z-
dc.description.provenanceMade available in DSpace on 2014-12-02T16:29:41Z (GMT). No. of bitstreams: 1 WOSA1996VG69700015.pdf: 708993 bytes, checksum: a812cf94870f8693ea0f0007a62d8dc2 (MD5) Previous issue date: 1996 Bitstreams deleted on 2020-05-18T20:41:09Z: WOSA1996VG69700015.pdf,. Added 1 bitstream(s) on 2020-05-19T14:30:59Z : No. of bitstreams: 2 A1996VG69700015.pdf: 780862 bytes, checksum: cd96f6f28768f8a70b30728fdd39f3ed (MD5) WOSA1996VG69700015.pdf.txt: 37096 bytes, checksum: 755f5a6433fa51760c7b78c63116f8e4 (MD5)en
dc.description.provenanceMade available in DSpace on 2015-11-26T17:08:47Z (GMT). No. of bitstreams: 2 WOSA1996VG69700015.pdf: 708993 bytes, checksum: a812cf94870f8693ea0f0007a62d8dc2 (MD5) WOSA1996VG69700015.pdf.txt: 37096 bytes, checksum: 755f5a6433fa51760c7b78c63116f8e4 (MD5) Previous issue date: 1996en
dc.identifier.urihttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/80578pt_BR
dc.identifier.urihttp://www.repositorio.unicamp.br/handle/REPOSIP/80578
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/80578-
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentDepartamento de Farmacologiapt_BR
dc.contributor.departmentDepartamento de Farmacologiapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.description.abstractalternative-
dc.identifier.sourceA1996VG69700015-
dc.creator.orcid0000-0002-2817-2766pt_BR
dc.creator.orcid0000-0003-2201-8247pt_BR
dc.creator.orcid0000-0002-4346-7941pt_BR
dc.type.formArtigo originalpt_BR
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