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Article: Ability of sickle cells to scavenge endothelium-derived nitric oxide is reduced

TitleAbility of sickle cells to scavenge endothelium-derived nitric oxide is reduced
Authors
Issue Date2002
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.html
Citation
Acta Pharmacologica Sinica, 2002, v. 23 n. 11, p. 967-973 How to Cite?
AbstractAIM: To assess the ability of sickle cells to interfere with the release or transfer of endothelium-derived relaxing factor (EDRF) in comparison to normal erythrocytes. METHODS: A perfusion-superfusion bioassay system was used a canine carotid artery with endothelium (donor of EDRF) and a ring of the same vessel without endothelium (detector) were separated by tubing resulting in a five second interval for transfer of EDRF from donor to detector. Changes in isometric tension were monitored in both the donor and the detector preparations. Release of EDRF, as determined by sustained relaxations during the contractions to phenylephrine, was induced by infusing acetylcholine through the donor artery. RESULTS: Superfusion with normal and sickle erythrocytes caused impairment of the endothelium-dependent relaxations in both detector and donor tissues. When infused through the transfer line, sickle cells were less potent than normal erythrocytes in inhibiting relaxation in the detector tissues. In contrast, infusion of either normal erythrocytes or sickle cell through the donor artery caused similar degrees of inhibition in donor and detector arteries. Hemolysates from both types of erythrocytes were equieffective at either site of infusion. CONCLUSION: These results indicate that sickle cells are intrinsically less potent scavengers of EDRF than normal erythrocytes. However, exposure to the endothelium enhances the ability of sickle cells to inhibit lumenal release of endothelium-derived relaxing factor.
Persistent Identifierhttp://hdl.handle.net/10722/171284
ISSN
2015 Impact Factor: 3.166
2015 SCImago Journal Rankings: 1.161
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorOlmos, Len_US
dc.contributor.authorMombouli, JVen_US
dc.contributor.authorWasserstrum, Nen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:13:10Z-
dc.date.available2012-10-30T06:13:10Z-
dc.date.issued2002en_US
dc.identifier.citationActa Pharmacologica Sinica, 2002, v. 23 n. 11, p. 967-973en_US
dc.identifier.issn1671-4083en_US
dc.identifier.urihttp://hdl.handle.net/10722/171284-
dc.description.abstractAIM: To assess the ability of sickle cells to interfere with the release or transfer of endothelium-derived relaxing factor (EDRF) in comparison to normal erythrocytes. METHODS: A perfusion-superfusion bioassay system was used a canine carotid artery with endothelium (donor of EDRF) and a ring of the same vessel without endothelium (detector) were separated by tubing resulting in a five second interval for transfer of EDRF from donor to detector. Changes in isometric tension were monitored in both the donor and the detector preparations. Release of EDRF, as determined by sustained relaxations during the contractions to phenylephrine, was induced by infusing acetylcholine through the donor artery. RESULTS: Superfusion with normal and sickle erythrocytes caused impairment of the endothelium-dependent relaxations in both detector and donor tissues. When infused through the transfer line, sickle cells were less potent than normal erythrocytes in inhibiting relaxation in the detector tissues. In contrast, infusion of either normal erythrocytes or sickle cell through the donor artery caused similar degrees of inhibition in donor and detector arteries. Hemolysates from both types of erythrocytes were equieffective at either site of infusion. CONCLUSION: These results indicate that sickle cells are intrinsically less potent scavengers of EDRF than normal erythrocytes. However, exposure to the endothelium enhances the ability of sickle cells to inhibit lumenal release of endothelium-derived relaxing factor.en_US
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.htmlen_US
dc.relation.ispartofActa Pharmacologica Sinicaen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnemia, Sickle Cell - Metabolism - Pathologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium-Dependent Relaxing Factors - Metabolismen_US
dc.subject.meshErythrocytes - Metabolismen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshOxyhemoglobins - Metabolismen_US
dc.subject.meshPhenylephrine - Pharmacologyen_US
dc.subject.meshPregnancyen_US
dc.titleAbility of sickle cells to scavenge endothelium-derived nitric oxide is reduceden_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid12421471-
dc.identifier.scopuseid_2-s2.0-0036843943en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036843943&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume23en_US
dc.identifier.issue11en_US
dc.identifier.spage967en_US
dc.identifier.epage973en_US
dc.identifier.isiWOS:000179049300002-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridOlmos, L=7005286818en_US
dc.identifier.scopusauthoridMombouli, JV=7004285772en_US
dc.identifier.scopusauthoridWasserstrum, N=7004673923en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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