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Article: Time course of coronary endothelial dysfunction in acute untreated rejection after heterotopic heart transplantation

TitleTime course of coronary endothelial dysfunction in acute untreated rejection after heterotopic heart transplantation
Authors
Issue Date1997
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/healun
Citation
Journal Of Heart And Lung Transplantation, 1997, v. 16 n. 6, p. 643-657 How to Cite?
AbstractBackground: Endothelial dysfunction is one of the early events leading to atherosclerosis. It occurs early after orthotopic heart transplantation and precedes the appearance of accelerated graft coronary artery disease believed to stem from chronic rejection of the endothelium. Acute rejection may contribute to the development of graft vasculopathy. Methods: To assess the time course and specific mechanisms of coronary endothelial dysfunction in acute untreated rejection, a swine model of retroperitoneal heterotopic heart transplantation was used. Large white swine (age 10 ± 2 weeks, weight 25 ± 5 kg) were serum-typed for class I antigen of the swine leukocyte antigen system and selected to ensure a similar degree of incompatibility. Donor hearts were preserved with normothermic blood cardioplegia and regional hypothermia; the mean ischemic time was 64 ± 15 minutes. Myocardial contractility decreased from day 5 (normal) to day 14 (weak), but electrical activity was preserved. All coronary arteries were patent, and International Society for Heart and Lung Transplantation grade 4 rejection was present in all hearts beyond 5 days. The endothelial function of epicardial coronary arterial rings of native and transplanted hearts was studied in organ chambers filled with modified Krebs-Ringer bicarbonate solution and compared 1, 5, 9, and 14 days after transplantation. Results: Maximal endothelium- independent relaxations were unaffected at all stages. Endothelium-dependent relaxations to serotonin and α2-adrenergic agonist UK 14304 (which activate receptors coupled to Gi-proteins) and to sodium fluoride (a direct G-protein activator) deteriorated progressively over time. At 14 days maximal relaxations to the calcium ionophore A23187, adenosine diphosphate, and bradykinin were also reduced, but to a lesser degree than those to serotonin and sodium fluoride. Histomorphometric studies of the allograft coronary artery rings showed progressive intimal hyperplasia from day 5 to day 14, with an increase in the incidence from 29% ± 8.3% to 61.5% ±12%. Conclusions: These studies show that endothelial dysfunction in untreated acute rejection after heart transplantation develops beyond 5 days and initially involves G-proteins; the dysfunction worsens over time to finally affect all endothelial mechanisms and vascular smooth muscle. The progression of the associated intimal hyperplasia parallels the alteration in endothelial function, suggesting a permissive role of the dysfunction in the development of this acute form of coronary graft vasculopathy.
Persistent Identifierhttp://hdl.handle.net/10722/171197
ISSN
2015 Impact Factor: 7.509
2015 SCImago Journal Rankings: 3.655
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorPerrault, LPen_US
dc.contributor.authorBidouard, JPen_US
dc.contributor.authorJaniak, Pen_US
dc.contributor.authorVilleneuve, Nen_US
dc.contributor.authorBruneval, Pen_US
dc.contributor.authorVilaine, JPen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:38Z-
dc.date.available2012-10-30T06:12:38Z-
dc.date.issued1997en_US
dc.identifier.citationJournal Of Heart And Lung Transplantation, 1997, v. 16 n. 6, p. 643-657en_US
dc.identifier.issn1053-2498en_US
dc.identifier.urihttp://hdl.handle.net/10722/171197-
dc.description.abstractBackground: Endothelial dysfunction is one of the early events leading to atherosclerosis. It occurs early after orthotopic heart transplantation and precedes the appearance of accelerated graft coronary artery disease believed to stem from chronic rejection of the endothelium. Acute rejection may contribute to the development of graft vasculopathy. Methods: To assess the time course and specific mechanisms of coronary endothelial dysfunction in acute untreated rejection, a swine model of retroperitoneal heterotopic heart transplantation was used. Large white swine (age 10 ± 2 weeks, weight 25 ± 5 kg) were serum-typed for class I antigen of the swine leukocyte antigen system and selected to ensure a similar degree of incompatibility. Donor hearts were preserved with normothermic blood cardioplegia and regional hypothermia; the mean ischemic time was 64 ± 15 minutes. Myocardial contractility decreased from day 5 (normal) to day 14 (weak), but electrical activity was preserved. All coronary arteries were patent, and International Society for Heart and Lung Transplantation grade 4 rejection was present in all hearts beyond 5 days. The endothelial function of epicardial coronary arterial rings of native and transplanted hearts was studied in organ chambers filled with modified Krebs-Ringer bicarbonate solution and compared 1, 5, 9, and 14 days after transplantation. Results: Maximal endothelium- independent relaxations were unaffected at all stages. Endothelium-dependent relaxations to serotonin and α2-adrenergic agonist UK 14304 (which activate receptors coupled to Gi-proteins) and to sodium fluoride (a direct G-protein activator) deteriorated progressively over time. At 14 days maximal relaxations to the calcium ionophore A23187, adenosine diphosphate, and bradykinin were also reduced, but to a lesser degree than those to serotonin and sodium fluoride. Histomorphometric studies of the allograft coronary artery rings showed progressive intimal hyperplasia from day 5 to day 14, with an increase in the incidence from 29% ± 8.3% to 61.5% ±12%. Conclusions: These studies show that endothelial dysfunction in untreated acute rejection after heart transplantation develops beyond 5 days and initially involves G-proteins; the dysfunction worsens over time to finally affect all endothelial mechanisms and vascular smooth muscle. The progression of the associated intimal hyperplasia parallels the alteration in endothelial function, suggesting a permissive role of the dysfunction in the development of this acute form of coronary graft vasculopathy.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/healunen_US
dc.relation.ispartofJournal of Heart and Lung Transplantationen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCoronary Disease - Pathology - Physiopathologyen_US
dc.subject.meshCoronary Vessels - Pathology - Physiologyen_US
dc.subject.meshElectrocardiographyen_US
dc.subject.meshEndothelium, Vascular - Pathology - Physiopathologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshFibromuscular Dysplasia - Pathology - Physiopathologyen_US
dc.subject.meshGraft Rejection - Pathology - Physiopathologyen_US
dc.subject.meshHeart Transplantation - Pathology - Physiologyen_US
dc.subject.meshMaleen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.subject.meshNitric Oxide Synthase - Physiologyen_US
dc.subject.meshSwineen_US
dc.subject.meshTransplantation, Heterotopic - Pathology - Physiologyen_US
dc.subject.meshVasodilation - Physiologyen_US
dc.titleTime course of coronary endothelial dysfunction in acute untreated rejection after heterotopic 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.pmid9229295-
dc.identifier.scopuseid_2-s2.0-0030759430en_US
dc.identifier.volume16en_US
dc.identifier.issue6en_US
dc.identifier.spage643en_US
dc.identifier.epage657en_US
dc.identifier.isiWOS:A1997XK17200009-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridPerrault, LP=7004370552en_US
dc.identifier.scopusauthoridBidouard, JP=6601955808en_US
dc.identifier.scopusauthoridJaniak, P=6603686655en_US
dc.identifier.scopusauthoridVilleneuve, N=7003458215en_US
dc.identifier.scopusauthoridBruneval, P=35414804500en_US
dc.identifier.scopusauthoridVilaine, JP=7004617134en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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