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Am J Cardiol. 2000 Feb 1;85(3):381-5.

Resistance vessel endothelial function in healthy humans during transient postprandial hypertriglyceridemia.

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Department of Internal Medicine, General Clinical Research Center, University of Iowa Hospitals and Clinics, Iowa City 52242, USA.


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.

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