dc.creatorMARIANIPEDROSO, SR
dc.creatorBIZETO, L
dc.creatorANTUNES, E
dc.creatorZATZ, R
dc.creatorDENUCCI, G
dc.date1995
dc.dateJUN
dc.date2014-12-16T11:37:17Z
dc.date2015-11-26T16:26:23Z
dc.date2014-12-16T11:37:17Z
dc.date2015-11-26T16:26:23Z
dc.date.accessioned2018-03-28T23:07:10Z
dc.date.available2018-03-28T23:07:10Z
dc.identifierProstaglandins Leukotrienes And Essential Fatty Acids. Churchill Livingstone, v. 52, n. 6, n. 399, n. 402, 1995.
dc.identifier0952-3278
dc.identifierWOS:A1995RB39400007
dc.identifier10.1016/0952-3278(95)90068-3
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/62532
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/62532
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/62532
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1268875
dc.descriptionThe ability of prostaglandin E(1) (PGE(1)) and nitric oxide (NO) donor compounds such as sodium nitroprusside (SNP), glyceryl trinitrate (GTN), and 3-morpholino-sydnonimine (SIN-1) to modulate the histamine- and bradykinin-induced increase in microvascular permeability have been investigated in rabbit skin, The effect of the NO synthesis inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME) on the plasma exudation induced by histamine and bradykinin was also studied. Local edema formation was evaluated using [I-125]human serum albumin, New Zealand white rabbits received an intravenous injection of [I-125]human albumin followed immediately by the intradermal injection of edematogenic agents into the shaved dorsolateral skin. PGE(1) (0.1 nmol/site) significantly potentiated both histamine- and bradykinin-induced edema. In contrast, SNP (0.4-400 nmol/site), SIN-1 (0.4-400 nmol/site), and GTN (0.4-40 nmol/site) did not affect the edematogenic response induced by either histamine or bradykinin. GTN (0.4-40 nmol/site) also had no effect on the increase in plasma exudation induced by histamine and bradykinin in the presence of PGE(1). L-NAME (50-400 nmol/site), but not its enantiomer D-NAME, dose-dependently reduced the edema formation induced by a combination of either histamine or bradykinin with PGE(1). This inhibition was significantly reversed by SNP (4-400 nmol/site) and by high doses (2.5 mu mol/site) of L-arginine (but not by D-arginine). Our results thus demonstrate that PGE(1), but not nitrovasodilators, can actually potentiate histamine- and bradykinin-induced edema in rabbit skin. This discrepancy cannot be explained by the lack of vasodilator activity of the nitrovasodilators since these were able to reverse the L-NAME-induced inhibition of the edema provoked by histamine. Rather, this difference most likely reflects the ability of PGE(1) to modulate vascular permeability by mechanism(s) other than an increase in arterial flow.
dc.description52
dc.description6
dc.description399
dc.description402
dc.languageen
dc.publisherChurchill Livingstone
dc.publisherEdinburgh
dc.publisherEscócia
dc.relationProstaglandins Leukotrienes And Essential Fatty Acids
dc.relationProstaglandins Leukot. Essent. Fatty Acids
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectIncreased Vascular-permeability
dc.subjectPlatelet-activating Factor
dc.subjectGene-related Peptide
dc.subjectGuinea-pig Skin
dc.subjectSubstance-p
dc.subjectRelaxing Factor
dc.subjectCanine Forelimb
dc.subjectEdema Formation
dc.subjectInflammation
dc.subjectInhibition
dc.titleDISSIMILARITY BETWEEN PROSTAGLANDIN E(1) AND NITRIC-OXIDE DONORS AS POTENTIATORS OF PLASMA EXUDATION IN THE RABBIT SKIN IN-VIVO
dc.typeArtículos de revistas


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