dc.creatorFerreira, HHA
dc.creatorMedeiros, MV
dc.creatorLima, CSP
dc.creatorFlores, CA
dc.creatorSannomiya, P
dc.creatorAntunes, E
dc.creatorDeNucci, G
dc.date1996
dc.dateAUG 29
dc.date2014-12-02T16:29:41Z
dc.date2015-11-26T17:08:47Z
dc.date2014-12-02T16:29:41Z
dc.date2015-11-26T17:08:47Z
dc.date.accessioned2018-03-28T23:57:27Z
dc.date.available2018-03-28T23:57:27Z
dc.identifierEuropean Journal Of Pharmacology. Elsevier Science Bv, v. 310, n. 41700, n. 201, n. 207, 1996.
dc.identifier0014-2999
dc.identifierWOS:A1996VG69700015
dc.identifier10.1016/0014-2999(96)00379-2
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/80578
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/80578
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/80578
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1280462
dc.descriptionThe 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 eosinophils.
dc.description310
dc.description41700
dc.description201
dc.description207
dc.languageen
dc.publisherElsevier Science Bv
dc.publisherAmsterdam
dc.publisherHolanda
dc.relationEuropean Journal Of Pharmacology
dc.relationEur. J. Pharmacol.
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectN-omega-nitro-L-arginine methyl ester
dc.subjecteosinophil chemotaxis
dc.subjectnitric oxide (NO)
dc.subjectpleurisy
dc.subjectcGMP
dc.subjectPlatelet-activating-factor
dc.subjectVascular Smooth-muscle
dc.subjectRelaxing Factor
dc.subjectCyclic-gmp
dc.subjectPharmacological Modulation
dc.subjectTrypanosoma-cruzi
dc.subjectHuman-neutrophils
dc.subjectGuinea-pig
dc.subjectL-arginine
dc.subjectIn-vitro
dc.titleInhibition of eosinophil chemotaxis by chronic blockade of nitric oxide biosynthesis
dc.typeArtículos de revistas


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