File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Endothelial dysfunction and coronary heart disease. Interaction of endothelium and thrombocytes | Endotheliale Dysfunktion und koronare Herzkrankheit. Interaktion von Endothel und Thrombozyten.

TitleEndothelial dysfunction and coronary heart disease. Interaction of endothelium and thrombocytes | Endotheliale Dysfunktion und koronare Herzkrankheit. Interaktion von Endothel und Thrombozyten.
Authors
Issue Date1993
PublisherVerlag Hans Huber AG. The Journal's web site is located at http://www.praxis.ch
Citation
Schweizerische Rundschau Fur Medizin Praxis = Revue Suisse De Medecine Praxis, 1993, v. 82 n. 42, p. 1161-1166 How to Cite?
AbstractAggregating thrombocytes release various mediators acting on endothelium and muscle cells of coronary arteries. In coronary arteries without endothelium, platelets induce potent vasoconstriction, whereas in segments with endothelium platelets induce relaxation. This endothelium-dependent relaxation induced by platelets is caused by the endothelial relaxation factor EDRF or nitric oxide (NO). NO inhibits not only smooth muscle cells of the vessels but also platelets themselves, an effect which is potentiated by prostacyclin. The physiologic importance of platelets-mediated contraction after removal of the vascular endothelium concerns the vascular phase of hemostasis. With the appearance of functional endothelial disorders, particularly in patients with cardiovascular risk factors, disturbances of coronary circulation can arise and finally cause ischemia. The finding that regenerated endothelial cells show functional defects especially towards the action of platelets (mainly the serotonin released from platelets) is important. In this functional disorder a dysfunction of Gi-protein of the endothelial 5HT1-serotonergic receptor plays a decisive role. Similar functional endothelial disorders can be shown after ischemia and reperfusion as well as in arteriosclerosis.
Persistent Identifierhttp://hdl.handle.net/10722/171117
ISSN
2011 SCImago Journal Rankings: 0.107

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:15Z-
dc.date.available2012-10-30T06:12:15Z-
dc.date.issued1993en_US
dc.identifier.citationSchweizerische Rundschau Fur Medizin Praxis = Revue Suisse De Medecine Praxis, 1993, v. 82 n. 42, p. 1161-1166en_US
dc.identifier.issn1013-2058en_US
dc.identifier.urihttp://hdl.handle.net/10722/171117-
dc.description.abstractAggregating thrombocytes release various mediators acting on endothelium and muscle cells of coronary arteries. In coronary arteries without endothelium, platelets induce potent vasoconstriction, whereas in segments with endothelium platelets induce relaxation. This endothelium-dependent relaxation induced by platelets is caused by the endothelial relaxation factor EDRF or nitric oxide (NO). NO inhibits not only smooth muscle cells of the vessels but also platelets themselves, an effect which is potentiated by prostacyclin. The physiologic importance of platelets-mediated contraction after removal of the vascular endothelium concerns the vascular phase of hemostasis. With the appearance of functional endothelial disorders, particularly in patients with cardiovascular risk factors, disturbances of coronary circulation can arise and finally cause ischemia. The finding that regenerated endothelial cells show functional defects especially towards the action of platelets (mainly the serotonin released from platelets) is important. In this functional disorder a dysfunction of Gi-protein of the endothelial 5HT1-serotonergic receptor plays a decisive role. Similar functional endothelial disorders can be shown after ischemia and reperfusion as well as in arteriosclerosis.en_US
dc.languageengen_US
dc.publisherVerlag Hans Huber AG. The Journal's web site is located at http://www.praxis.chen_US
dc.relation.ispartofSchweizerische Rundschau fur Medizin Praxis = Revue suisse de medecine Praxisen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlood Platelets - Physiologyen_US
dc.subject.meshCoronary Circulation - Physiologyen_US
dc.subject.meshCoronary Disease - Physiopathologyen_US
dc.subject.meshEndothelium, Vascular - Physiopathologyen_US
dc.subject.meshEpoprostenol - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.subject.meshPlatelet Aggregation - Physiologyen_US
dc.titleEndothelial dysfunction and coronary heart disease. Interaction of endothelium and thrombocytes | Endotheliale Dysfunktion und koronare Herzkrankheit. Interaktion von Endothel und Thrombozyten.en_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.pmid8248687-
dc.identifier.scopuseid_2-s2.0-0027920493en_US
dc.identifier.volume82en_US
dc.identifier.issue42en_US
dc.identifier.spage1161en_US
dc.identifier.epage1166en_US
dc.publisher.placeSwitzerlanden_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats