Document Detail


Resistance vessel endothelial function in healthy humans during transient postprandial hypertriglyceridemia.
MedLine Citation:
PMID:  11078311     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A single high-fat meal transiently impairs conduit vessel endothelial function. We tested the hypothesis that transient moderate hypertriglyceridemia by consumption of a high-fat meal impairs forearm resistance vessel endothelial function. Fifteen healthy persons consumed isocaloric high- and low-fat meals (900 calories, 50 and 4 g of fat, respectively) on 2 separate days. Endothelial function in forearm resistance vessels was assessed using blood flow responses to local intra-arterial infusion of nitroprusside, acetylcholine, bradykinin, and verapamil from 1 to 3 hours after the meal. Serum triglycerides increased from 112 +/- 15 mg/dl preprandially to 165 +/- 20 mg/dl 4 hours after the high-fat meal, which was a significantly larger increase than levels after the low-fat meal (p = 0.01). Total cholesterol, high-density lipoprotein, low-density lipoprotein, and very low density lipoprotein (VLDL) cholesterol concentrations did not change. There was no difference between high- and low-fat meals in vasodilation to the endothelium-dependent agents acetylcholine (low fat, 337 +/- 47%; high fat, 356 +/- 88%; p = 0.81) and bradykinin (low fat, 312 +/- 39%; high fat, 403 +/- 111%; p = 0.28), or to the endothelium-independent vasodilators nitroprusside (low fat, 313 +/- 27%; high fat, 355 +/- 42%; p = 0.31) and verapamil (low fat, 292 +/- 48%; high fat, 299 +/- 36%; p = 0.18). Thus, transient hypertriglyceridemia due to a high-fat meal does not impair resistance vessel endothelial function. These data contrast with previous studies in conduit vessels that showed substantial endothelial dysfunction. Therefore, although high-fat intake may contribute to large artery atherosclerosis, it probably does not predispose to hypertension or ischemia through resistance vessel dysfunction. The results suggest that the mechanism by which triglyceride-rich lipoproteins impair endothelial function in conduit vessels is not operative in resistance vessels.
Authors:
G S Gudmundsson; C A Sinkey; C A Chenard; P J Stumbo; W G Haynes
Publication Detail:
Type:  Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of cardiology     Volume:  85     ISSN:  0002-9149     ISO Abbreviation:  Am. J. Cardiol.     Publication Date:  2000 Feb 
Date Detail:
Created Date:  2000-11-15     Completed Date:  2000-11-30     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0207277     Medline TA:  Am J Cardiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  381-5     Citation Subset:  AIM; IM    
Affiliation:
Department of Internal Medicine, General Clinical Research Center, University of Iowa Hospitals and Clinics, Iowa City 52242, USA.
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MeSH Terms
Descriptor/Qualifier:
Acetylcholine / pharmacology
Adult
Bradykinin / pharmacology
Cross-Over Studies
Dietary Fats / administration & dosage*
Dose-Response Relationship, Drug
Double-Blind Method
Endothelium, Vascular / drug effects,  physiology*
Forearm / blood supply
Humans
Hypertriglyceridemia / physiopathology*
Male
Nitroprusside / pharmacology
Postprandial Period
Reference Values
Regional Blood Flow
Triglycerides / blood
Vascular Resistance / drug effects*
Vasodilator Agents / pharmacology*
Verapamil / pharmacology
Grant Support
ID/Acronym/Agency:
HL14388/HL/NHLBI NIH HHS; HL58972/HL/NHLBI NIH HHS; RR00059/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Dietary Fats; 0/Triglycerides; 0/Vasodilator Agents; 15078-28-1/Nitroprusside; 51-84-3/Acetylcholine; 52-53-9/Verapamil; 58-82-2/Bradykinin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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