Title of article
Resistance vessel endothelial function in healthy humans during transient postprandial hypertriglyceridemia
Author/Authors
Gudmundsson، نويسنده , , G.Steinar and Sinkey، نويسنده , , Christine A and Chenard، نويسنده , , Catherine A and Stumbo، نويسنده , , Phyllis J and Haynes، نويسنده , , William G، نويسنده ,
Issue Information
روزنامه با شماره پیاپی سال 2000
Pages
5
From page
381
To page
385
Abstract
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.
Journal title
American Journal of Cardiology
Serial Year
2000
Journal title
American Journal of Cardiology
Record number
1891769
Link To Document