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Article: Mechanisms responsible for coronary vasospasm

TitleMechanisms responsible for coronary vasospasm
Authors
Issue Date1986
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/jac
Citation
Journal Of The American College Of Cardiology, 1986, v. 8 n. 1 SUPPL. A, p. 50A-54A How to Cite?
AbstractStudies have been conducted on isolated segments of the left circumflex coronary artery of the dog to gain information on the mechanism or mechanisms of vasospasm. Coronary arteries contain both postjunctional alpha1- and beta1-adrenoceptors, and both are accessible to norepinephrine released from the sympathetic nerves. However, owing to the dominance of the beta1-adrenoceptors, sympathetic stimulation causes relaxation of the vascular smooth muscle. In the primary branches of the circumflex artery, only beta1-adrenoceptors are present. In patients with spasm of the coronary arteries, blockade of the beta1-adrenoceptors may aggravate the spasm by permitting the unopposed constrictor action of the sympathetic nerves on the alpha1-adrenoceptors on these vessels. The blood platelets contain substances, including 5-hydroxytryptamine (serotonin) and thromboxane A2, which can cause constriction of vascular smooth muscle. These substances are released whenever platelets aggregate. The normal endothelium, by forming and releasing prostacyclin, inhibits platelet aggregation. In addition, in response to platelet products, the normal endothelium forms one or more inhibitory substances that cause relaxation of the underlying smooth muscle. Also, if any thrombin is formed, this also causes an endothelium-mediated relaxation of the artery. Patients with coronary artery spasm usually have morphologic changes in the artery at the site of the spasm. Thus, platelets can aggregate at the site and the resultant release of serotonin and thromboxane A2, acting directly on the smooth muscle, causes constriction of the artery. Hypoxia of the myocardium follows and this augments the constriction.
Persistent Identifierhttp://hdl.handle.net/10722/170810
ISSN
2015 Impact Factor: 17.759
2015 SCImago Journal Rankings: 10.097
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorShepherd, Ten_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:57Z-
dc.date.available2012-10-30T06:10:57Z-
dc.date.issued1986en_US
dc.identifier.citationJournal Of The American College Of Cardiology, 1986, v. 8 n. 1 SUPPL. A, p. 50A-54Aen_US
dc.identifier.issn0735-1097en_US
dc.identifier.urihttp://hdl.handle.net/10722/170810-
dc.description.abstractStudies have been conducted on isolated segments of the left circumflex coronary artery of the dog to gain information on the mechanism or mechanisms of vasospasm. Coronary arteries contain both postjunctional alpha1- and beta1-adrenoceptors, and both are accessible to norepinephrine released from the sympathetic nerves. However, owing to the dominance of the beta1-adrenoceptors, sympathetic stimulation causes relaxation of the vascular smooth muscle. In the primary branches of the circumflex artery, only beta1-adrenoceptors are present. In patients with spasm of the coronary arteries, blockade of the beta1-adrenoceptors may aggravate the spasm by permitting the unopposed constrictor action of the sympathetic nerves on the alpha1-adrenoceptors on these vessels. The blood platelets contain substances, including 5-hydroxytryptamine (serotonin) and thromboxane A2, which can cause constriction of vascular smooth muscle. These substances are released whenever platelets aggregate. The normal endothelium, by forming and releasing prostacyclin, inhibits platelet aggregation. In addition, in response to platelet products, the normal endothelium forms one or more inhibitory substances that cause relaxation of the underlying smooth muscle. Also, if any thrombin is formed, this also causes an endothelium-mediated relaxation of the artery. Patients with coronary artery spasm usually have morphologic changes in the artery at the site of the spasm. Thus, platelets can aggregate at the site and the resultant release of serotonin and thromboxane A2, acting directly on the smooth muscle, causes constriction of the artery. Hypoxia of the myocardium follows and this augments the constriction.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/jacen_US
dc.relation.ispartofJournal of the American College of Cardiologyen_US
dc.subject.meshAdenosine Diphosphate - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCoronary Vasospasm - Etiologyen_US
dc.subject.meshDinoprosten_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium - Metabolismen_US
dc.subject.meshEpoprostenol - Biosynthesisen_US
dc.subject.meshHeart - Innervationen_US
dc.subject.meshHumansen_US
dc.subject.meshMuscle, Smooth, Vascular - Metabolismen_US
dc.subject.meshPlatelet Aggregationen_US
dc.subject.meshProstaglandins F - Metabolismen_US
dc.subject.meshReceptors, Adrenergic - Drug Effects - Metabolismen_US
dc.subject.meshSerotonin - Metabolismen_US
dc.subject.meshSwineen_US
dc.subject.meshSwine, Miniatureen_US
dc.subject.meshSympathetic Nervous System - Metabolismen_US
dc.subject.meshThromboxane A2 - Metabolismen_US
dc.titleMechanisms responsible for coronary vasospasmen_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.doi10.1016/S0735-1097(86)80028-6-
dc.identifier.pmid3519733-
dc.identifier.scopuseid_2-s2.0-0022475865en_US
dc.identifier.volume8en_US
dc.identifier.issue1 SUPPL. Aen_US
dc.identifier.spage50Aen_US
dc.identifier.epage54Aen_US
dc.identifier.isiWOS:A1986C926600007-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridShepherd, T=7103294744en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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