Linked Life Data

19546816

Source:http://linkedlifedata.com/resource/pubmed/id/19546816

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-7-21
pubmed:abstractText
The aim of this study was to evaluate the role of cyclooxygenase (COX) in venous vascular reactivity changes after an oral lipid overload (OLO). Venous endothelial function (dorsal hand vein technique) was evaluated in fasting, 30 minutes after COX inhibition (aspirin-fasting), 2 to 4 hours after an OLO (1000 kcal, 58% fat), and again after COX inhibition (aspirin-OLO, 600 mg/200 mL water) in 10 healthy adults (age, 28.1 +/- 1.3 years; body mass index, 22.3 +/- 0.6 kg/m). Fasting, 2- to 4-hour post-OLO, and 60-minute postaspirin plasma glucose, insulin, and lipids were also evaluated. The OLO increased triglycerides and insulin, reduced low-density lipoprotein and high-density lipoprotein, but glycemia and total cholesterol remained unchanged. There were no metabolic differences between OLO and aspirin-OLO. In fasting, aspirin reduced acetylcholine-induced venodilation (107.0% +/- 14% versus 57.3% +/- 11%; P < 0.001). Vascular reactivity was blunted after the OLO (phenylephrine dose: 0.3 +/- 0.2 fasting versus 1.9 +/- 0.8 nmol/min after OLO; P < 0.001) and was partially corrected by aspirin (0.4 +/- 0.2; P < 0.001). Similar changes were observed in maximum venodilation after acetylcholine (107.0% +/- 14% fasting versus 60.4% +/- 9% after OLO, P < 0.001; aspirin-OLO: 95.9% +/- 6%; P < 0.001). The responses to sodium nitroprusside remained unchanged during the study. We conclude that the OLO reduction in the endothelium-dependent venoconstriction and venodilation is partially the result of the action of COX.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1533-4023
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
90-3
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:19546816-Acetylcholine, pubmed-meshheading:19546816-Adult, pubmed-meshheading:19546816-Aspirin, pubmed-meshheading:19546816-Blood Glucose, pubmed-meshheading:19546816-Body Mass Index, pubmed-meshheading:19546816-Cholesterol, HDL, pubmed-meshheading:19546816-Cholesterol, LDL, pubmed-meshheading:19546816-Cyclooxygenase Inhibitors, pubmed-meshheading:19546816-Endothelium, Vascular, pubmed-meshheading:19546816-Fasting, pubmed-meshheading:19546816-Humans, pubmed-meshheading:19546816-Hypoglycemic Agents, pubmed-meshheading:19546816-Insulin, pubmed-meshheading:19546816-Lipid Metabolism, pubmed-meshheading:19546816-Lipids, pubmed-meshheading:19546816-Male, pubmed-meshheading:19546816-Phenylephrine, pubmed-meshheading:19546816-Postprandial Period, pubmed-meshheading:19546816-Time Factors, pubmed-meshheading:19546816-Triglycerides, pubmed-meshheading:19546816-Vasodilation, pubmed-meshheading:19546816-Veins
pubmed:year
2009
pubmed:articleTitle
Reversal of postprandial endothelial dysfunction by cyclooxygenase inhibition in healthy volunteers.
pubmed:affiliation
Institute of Cardiology of Rio Grande do Sul/University Foundation of Cardiology, 370-Santana-Porto Alegre, RS-Brasil-90620-000.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't