File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Conference Paper: Mechanisms of coronary vasospasm: Role of endothelium

TitleMechanisms of coronary vasospasm: Role of endothelium
Authors
Issue Date1991
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmcc
Citation
Journal Of Molecular And Cellular Cardiology, 1991, v. 23 SUPPL. 1, p. 125-131 How to Cite?
AbstractStudies in recent years have demonstrated that coronary vasospasm (Prinzmetal's Angina) is a consequence of endothelial cell damage. Normal endothelium, in response to increases in shear stress, or to platelet products and other agonists, releases endothelium-derived relaxing factor(s) (EDRF) with resultant vasodilatation. One substance released may be nitric oxide, another a hyperpolarizing factor. In addition EDRF, like prostacyclin, inhibits platelet aggregation. In porcine coronary vessels the amount of EDRF released can be increased by a diet of codliver oil and decreased by a high cholesterol diet. When endothelium is damaged, the absence of EDRF and prostacyclin at the site leads to platelet aggregation with the release, among other substances, of serotonin (5HT) and thromboxane A2. These now act directly on the smooth muscle to cause contraction. In addition some serotonin is taken up by the sympathetic nerve endings and is released as a false transmitter to aggravate the constriction. The resultant hypoxia/anoxia can cause any functional endothelium to release contracting factor(s), further compounding the constriction. Evidence of platelet aggregation in humans is the presence of serotonin in the coronary sinus blood in resting patients with coronary artery disease.
Persistent Identifierhttp://hdl.handle.net/10722/173493
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.522
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSheperd, JTen_US
dc.contributor.authorKatusic, ZSen_US
dc.contributor.authorVedernikov, Yen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:20Z-
dc.date.available2012-10-30T06:32:20Z-
dc.date.issued1991en_US
dc.identifier.citationJournal Of Molecular And Cellular Cardiology, 1991, v. 23 SUPPL. 1, p. 125-131en_US
dc.identifier.issn0022-2828en_US
dc.identifier.urihttp://hdl.handle.net/10722/173493-
dc.description.abstractStudies in recent years have demonstrated that coronary vasospasm (Prinzmetal's Angina) is a consequence of endothelial cell damage. Normal endothelium, in response to increases in shear stress, or to platelet products and other agonists, releases endothelium-derived relaxing factor(s) (EDRF) with resultant vasodilatation. One substance released may be nitric oxide, another a hyperpolarizing factor. In addition EDRF, like prostacyclin, inhibits platelet aggregation. In porcine coronary vessels the amount of EDRF released can be increased by a diet of codliver oil and decreased by a high cholesterol diet. When endothelium is damaged, the absence of EDRF and prostacyclin at the site leads to platelet aggregation with the release, among other substances, of serotonin (5HT) and thromboxane A2. These now act directly on the smooth muscle to cause contraction. In addition some serotonin is taken up by the sympathetic nerve endings and is released as a false transmitter to aggravate the constriction. The resultant hypoxia/anoxia can cause any functional endothelium to release contracting factor(s), further compounding the constriction. Evidence of platelet aggregation in humans is the presence of serotonin in the coronary sinus blood in resting patients with coronary artery disease.en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmccen_US
dc.relation.ispartofJournal of Molecular and Cellular Cardiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Complicationsen_US
dc.subject.meshCoronary Vasospasm - Blood - Etiologyen_US
dc.subject.meshDieten_US
dc.subject.meshEndothelium, Vascular - Pathology - Physiopathologyen_US
dc.subject.meshHumansen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshReperfusion Injury - Complicationsen_US
dc.titleMechanisms of coronary vasospasm: Role of endotheliumen_US
dc.typeConference_Paperen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/0022-2828(91)90031-Gen_US
dc.identifier.pmid2038073-
dc.identifier.scopuseid_2-s2.0-0026021865en_US
dc.identifier.volume23en_US
dc.identifier.issueSUPPL. 1en_US
dc.identifier.spage125en_US
dc.identifier.epage131en_US
dc.identifier.isiWOS:A1991FD09500015-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridSheperd, JT=6603381819en_US
dc.identifier.scopusauthoridKatusic, ZS=7006971465en_US
dc.identifier.scopusauthoridVedernikov, Y=35461855900en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats