Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1998-4-9
pubmed:abstractText
Myocardial ischaemia and reperfusion cause dysfunction of the coronary vasculature leading to a sustained reduction in coronary blood flow and an impairment of responses to both endothelium-dependent and endothelium-independent vasodilators. In contrast, when previously ischaemic arteries are removed from the myocardium and vascular function is examined in vitro, it is evident that while endothelial function is impaired, smooth muscle reactivity remains intact. Therefore, other changes must be responsible for the general reduction in vasodilator reserve. Examination of the vasculature in the ischaemic myocardium by electron microscopy reveals adhesion of leukocytes and plugging of capillaries. There also is evidence that polymorphonuclear leukocytes (PMNs) release a factor that constricts coronary arterioles, and that release of this factor is increased by atherosclerosis. The identity of this factor remains uncertain, but the calcium antagonist amlodipine prevents the coronary vasoconstriction. Amlodipine is also able to prevent the impaired perfusion and the reduction in vasodilator reserve that occurs after myocardial ischaemia and reperfusion in the dog. In addition, amlodipine prevents the endothelial dysfunction observed in isolated arteries after ischaemia and reperfusion. The interaction between the endothelium and activated PMNs may be a suitable target for pharmacological intervention to improve postischaemic vascular function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0167-5273
pubmed:author
pubmed:issnType
Print
pubmed:day
31
pubmed:volume
62 Suppl 2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S91-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Prevention of ischaemia-induced coronary vascular dysfunction.
pubmed:affiliation
Department of Pharmacology, University of Melbourne, Parkville Victoria, Australia. o.woodman@pharmacology.unimelb.edu.au
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't