Linked Life Data

9231821

Source:http://linkedlifedata.com/resource/pubmed/id/9231821

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1 Pt 1
pubmed:dateCreated
1997-8-8
pubmed:abstractText
Hypercholesterolemic and hypertensive patients have impaired endothelium-dependent vasorelaxation because of decreased nitric oxide activity, but the mechanism underlying this abnormality is unknown. This study sought to determine whether an increased breakdown of nitric oxide by xanthine oxidase-generated superoxide anions could participate in these forms of endothelial dysfunction. We studied vascular responses to intrabrachial infusion of acetylcholine (an endothelium-dependent vasodilator, 7.5 to 30 microg/min) and sodium nitroprusside (a direct smooth muscle dilator, 0.8 to 3.2 microg/min) by strain-gauge plethysmography before and during the combined administration of oxypurinol (300 microg/min), a xanthine oxidase inhibitor, in 20 hypercholesterolemic patients, 20 essential hypertensive patients, and 20 normal subjects. The vasodilator response to acetylcholine was blunted in hypercholesterolemic (highest flow, 8.2+/-8 mL x min(-1) x dL(-1)) and hypertensive (8.5+/-4 mL x min(-1) x dL(-1)) patients compared with control subjects (13.8+/- 6.6 mL x min(-1) x dL(-1)) (both P<.001); however, no differences were observed in the response to sodium nitroprusside. Oxypurinol did not change the response to acetylcholine in control subjects (P=.26) and improved, but did not normalize, its vasodilator effect in hypercholesterolemic patients (P<.01). Oxypurinol did not affect the response to acetylcholine in hypertensive patients (P=.34) and did not modify the response to sodium nitroprusside in any group. These results suggest that xanthine oxidase-generated superoxide anions are partly responsible for the impaired endothelial vasodilator function of hypercholesterolemic patients. In contrast, this mechanism does not appear to play a significant role in essential hypertension.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0194-911X
pubmed:author
pubmed:issnType
Print
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
57-63
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:9231821-Acetylcholine, pubmed-meshheading:9231821-Analysis of Variance, pubmed-meshheading:9231821-Antihypertensive Agents, pubmed-meshheading:9231821-Endothelium, Vascular, pubmed-meshheading:9231821-Enzyme Inhibitors, pubmed-meshheading:9231821-Female, pubmed-meshheading:9231821-Forearm, pubmed-meshheading:9231821-Free Radicals, pubmed-meshheading:9231821-Humans, pubmed-meshheading:9231821-Hypercholesterolemia, pubmed-meshheading:9231821-Hypertension, pubmed-meshheading:9231821-Male, pubmed-meshheading:9231821-Middle Aged, pubmed-meshheading:9231821-Nitroprusside, pubmed-meshheading:9231821-Oxypurinol, pubmed-meshheading:9231821-Plethysmography, pubmed-meshheading:9231821-Vascular Resistance, pubmed-meshheading:9231821-Vasodilation, pubmed-meshheading:9231821-Vasodilator Agents, pubmed-meshheading:9231821-Xanthine Oxidase
pubmed:year
1997
pubmed:articleTitle
Xanthine oxidase inhibition with oxypurinol improves endothelial vasodilator function in hypercholesterolemic but not in hypertensive patients.
pubmed:affiliation
Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md 20892-1650, USA.
pubmed:publicationType
Journal Article, Comparative Study