dc.creatorCasarin, AL
dc.creatorLopes-Pires, ME
dc.creatorMorganti, RP
dc.creatorAntunes, E
dc.creatorMarcondes, S
dc.date2011
dc.date44501
dc.date2014-07-30T14:19:34Z
dc.date2015-11-26T17:41:06Z
dc.date2014-07-30T14:19:34Z
dc.date2015-11-26T17:41:06Z
dc.date.accessioned2018-03-29T00:22:51Z
dc.date.available2018-03-29T00:22:51Z
dc.identifierLife Sciences. Pergamon-elsevier Science Ltd, v. 89, n. 21-22, n. 773, n. 778, 2011.
dc.identifier0024-3205
dc.identifierWOS:000296932100004
dc.identifier10.1016/j.lfs.2011.09.004
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/58939
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/58939
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1286912
dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.descriptionAims: Excessive production of nitric oxide (NO) and reactive oxygen species (ROS) in sepsis modulates different cell functions. Since the sepsis severity is associated with the degree of platelet activation, we decided to investigate the role of systemic generation of NO and ROS in modulating the platelet adhesion of lipopolysaccharide (LPS)-treated rats. Main methods: Platelet adhesion was evaluated using fibrinogen-coated 96-well microtiter plates. Cyclic GMP levels were measured using enzyme immunoassay kit. Key findings: Treatment of rats with LPS significantly increased spontaneous platelet adhesion, but reduced the thrombin-activated platelet adhesion when compared with control rats. Chronic treatment of rats with the NO synthase inhibitor L-NAME (20 mg/rat/day, 7 days) prior to LPS injection normalized the increased adhesion in non-activated platelets, but failed to affect the adhesion in thrombin-activated platelets. The cGMP levels were modified neither in non-activated nor in thrombin-activated platelets of LPS-treated rats when compared with control rats. The incubation of non-activated platelets with the O-2(-) scavenger PEG-SOD reversed the stimulatory effect of LPS on spontaneous adhesion, but had no effect in stimulated-platelet adhesion of non-treated or LPS-treated groups. Moreover, pretreatment of rats with the antioxidant N-acetylcysteine (NAC: 150 mg/kg) prevented the increase of non-activated platelet adhesion, and significantly reduced the inhibitory effect of LPS on thrombin-stimulated adhesion. Significance: Our findings suggest that in LPS-treated rats, NO plays an important modulatory role only in non-stimulated platelet adhesion through cGMP-independent mechanisms, while ROS, directly or by affecting the redox state of the animals, modulates both non-activated and thrombin-activated platelet adhesion. (C) 2011 Elsevier Inc. All rights reserved.
dc.description89
dc.description21-22
dc.description773
dc.description778
dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.languageen
dc.publisherPergamon-elsevier Science Ltd
dc.publisherOxford
dc.publisherInglaterra
dc.relationLife Sciences
dc.relationLife Sci.
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectPlatelet adhesion
dc.subjectLipopolysaccharide
dc.subjectNitric oxide
dc.subjectOxidative stress
dc.subjectEscherichia-coli Lipopolysaccharide
dc.subjectDependent Protein-kinase
dc.subjectN-acetylcysteine
dc.subjectOxidative Stress
dc.subjectTyrosine Phosphorylation
dc.subjectIndependent Mechanisms
dc.subjectAntiplatelet Activity
dc.subjectSuperoxide Anion
dc.subjectBlood-platelets
dc.subjectCecal Ligation
dc.titleReactive oxygen and nitrogen species modulate the ex-vivo effects of LPS on platelet adhesion to fibrinogen
dc.typeArtículos de revistas


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