Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1991-7-3
pubmed:abstractText
Studies 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-2828
pubmed:author
pubmed:issnType
Print
pubmed:volume
23 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
125-31
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Mechanisms of coronary vasospasm: role of endothelium.
pubmed:affiliation
Mayo Clinic and Foundation, Rochester, Minnesota 55905.
pubmed:publicationType
Journal Article, Review