Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-2-22
pubmed:abstractText
Flow-mediated dilatation (FMD) of conduit arteries is dependent on an intact endothelium, although the mechanisms are not fully understood. Using high-resolution ultrasound, we examined the role of endothelial mediators in radial artery dilatation in response to transient (short period of reactive hyperemia) and sustained (prolonged period of reactive hyperemia, hand warming, or an incremental infusion of acetylcholine into the distal radial artery) hyperemia. After short episodes of reactive hyperemia, FMD was abolished by local infusion of the nitric oxide synthesis inhibitor N:(G)monomethyl-L-arginine (5.3+/-1.2% versus 0.7+/-0.7%, P:<0.001). In contrast, basal vessel diameter and dilatation after prolonged episodes of reactive hyperemia, hand warming, and distal infusion of acetylcholine were not attenuated by nitric oxide synthesis inhibition. Inhibition of cyclooxygenase or local autonomic nervous system blockade also had no effect on FMD. Patients with hypercholesterolemia exhibited reduced FMD in response to transient hyperemia, but the response to sustained hyperemia was normal. These data suggest heterogeneity of endothelial responses to blood flow that are dependent on the characteristics of the flow stimulus. Dilatation after brief episodes of hyperemia is mediated by release of nitric oxide, whereas dilatation during sustained hyperemia is unaffected by NO synthesis inhibition. Hypercholesterolemia seems to differentially affect these pathways with impairment of the nitric oxide-dependent pathway and preservation of non nitric oxide-mediated dilatation to sustained flow stimuli.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1524-4571
pubmed:author
pubmed:issnType
Electronic
pubmed:day
2
pubmed:volume
88
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
145-51
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11157665-Acetylcholine, pubmed-meshheading:11157665-Adolescent, pubmed-meshheading:11157665-Adult, pubmed-meshheading:11157665-Area Under Curve, pubmed-meshheading:11157665-Aspirin, pubmed-meshheading:11157665-Autonomic Agents, pubmed-meshheading:11157665-Blood Flow Velocity, pubmed-meshheading:11157665-Cyclooxygenase Inhibitors, pubmed-meshheading:11157665-Electrocardiography, pubmed-meshheading:11157665-Endothelium, Vascular, pubmed-meshheading:11157665-Enzyme Inhibitors, pubmed-meshheading:11157665-Female, pubmed-meshheading:11157665-Hand, pubmed-meshheading:11157665-Hot Temperature, pubmed-meshheading:11157665-Humans, pubmed-meshheading:11157665-Hypercholesterolemia, pubmed-meshheading:11157665-Hyperemia, pubmed-meshheading:11157665-Male, pubmed-meshheading:11157665-Middle Aged, pubmed-meshheading:11157665-Nitric Oxide, pubmed-meshheading:11157665-Radial Artery, pubmed-meshheading:11157665-Vasodilation, pubmed-meshheading:11157665-Vasodilator Agents, pubmed-meshheading:11157665-omega-N-Methylarginine
pubmed:year
2001
pubmed:articleTitle
Heterogenous nature of flow-mediated dilatation in human conduit arteries in vivo: relevance to endothelial dysfunction in hypercholesterolemia.
pubmed:affiliation
Vascular Physiology Unit, Institute of Child Health and the Centre for Clinical Pharmacology, University College London, London, UK. MichaelJMullen@cs.com
pubmed:publicationType
Journal Article, Clinical Trial, Controlled Clinical Trial, Research Support, Non-U.S. Gov't