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Article: The production of cyclic GMP decreases with the coronary endothelial dysfunction after heart transplantation

TitleThe production of cyclic GMP decreases with the coronary endothelial dysfunction after heart transplantation
Authors
Issue Date1997
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
Faseb Journal, 1997, v. 11 n. 3, p. A246 How to Cite?
AbstractA porcine model of heterotopic heart transplantation without immunosuppression was used to assess the mechanisms underlying the coronary endothelial dysfunction leading to coronary graft vasculopathy. Vascular reactivity studies showed a selective endothelial dysfunction to Giproteins mediated agonists thirty days after transplantation which became generalized to other pathways at sixty days. There was a progressive increase in the coronary intimal thickening in allografts from day thirty to day sixty. The addition of L-arginine (5mM) at the time of organ chambers experiments did not improve the endothelium-dependent relaxations to pertussis toxin-sensitive agonists. The basal production of cyclic guanosine monophosphate (GMP) was compared in native and allograft coronary arteries sixty days after transplantation. There was a statistically significant decrease of cyclic GMP release from the allograft coronary arteries compared to native arteries. This decrease in cyclic GMP is consistent with a decreased release or an increased degradation of nitric oxide underlying the coronary endothelial dsyfunction after heart transplantation Decreased availability of nitric oxide may contribute to graft coronary vasculopathy by favoring activation of adhesion molecules, platelet aggregation and proliferation of vascular smooth muscle cells.
Persistent Identifierhttp://hdl.handle.net/10722/171350
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorPerrault, LPen_US
dc.contributor.authorBidouard, JPen_US
dc.contributor.authorJacquemin, Cen_US
dc.contributor.authorPetit, Cen_US
dc.contributor.authorVilleneuve, Nen_US
dc.contributor.authorVilaine, JPen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:13:32Z-
dc.date.available2012-10-30T06:13:32Z-
dc.date.issued1997en_US
dc.identifier.citationFaseb Journal, 1997, v. 11 n. 3, p. A246en_US
dc.identifier.issn0892-6638en_US
dc.identifier.urihttp://hdl.handle.net/10722/171350-
dc.description.abstractA porcine model of heterotopic heart transplantation without immunosuppression was used to assess the mechanisms underlying the coronary endothelial dysfunction leading to coronary graft vasculopathy. Vascular reactivity studies showed a selective endothelial dysfunction to Giproteins mediated agonists thirty days after transplantation which became generalized to other pathways at sixty days. There was a progressive increase in the coronary intimal thickening in allografts from day thirty to day sixty. The addition of L-arginine (5mM) at the time of organ chambers experiments did not improve the endothelium-dependent relaxations to pertussis toxin-sensitive agonists. The basal production of cyclic guanosine monophosphate (GMP) was compared in native and allograft coronary arteries sixty days after transplantation. There was a statistically significant decrease of cyclic GMP release from the allograft coronary arteries compared to native arteries. This decrease in cyclic GMP is consistent with a decreased release or an increased degradation of nitric oxide underlying the coronary endothelial dsyfunction after heart transplantation Decreased availability of nitric oxide may contribute to graft coronary vasculopathy by favoring activation of adhesion molecules, platelet aggregation and proliferation of vascular smooth muscle cells.en_US
dc.languageengen_US
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/en_US
dc.relation.ispartofFASEB Journalen_US
dc.titleThe production of cyclic GMP decreases with the coronary endothelial dysfunction after heart transplantationen_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.scopuseid_2-s2.0-33750197416en_US
dc.identifier.volume11en_US
dc.identifier.issue3en_US
dc.identifier.spageA246en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridPerrault, LP=7004370552en_US
dc.identifier.scopusauthoridBidouard, JP=6601955808en_US
dc.identifier.scopusauthoridJacquemin, C=7004759803en_US
dc.identifier.scopusauthoridPetit, C=23103771000en_US
dc.identifier.scopusauthoridVilleneuve, N=7003458215en_US
dc.identifier.scopusauthoridVilaine, JP=7004617134en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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