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J Am Coll Cardiol, 2000; 36:417-422 © 2000 by the American College of Cardiology Foundation |
* Department of Cardiology, Royal Prince Alfred Hospital, Sydney, Australia
Department of Clinical Biochemistry, Royal Prince Alfred Hospital, Sydney, Australia
Department of Medicine, University of Sydney, Sydney, Australia
Department of Clinical Physiology, Turku University Central Hospital, Turku, Finland
Manuscript received October 25, 1999; revised manuscript received February 11, 2000, accepted March 30, 2000.
Reprint requests and correspondence: Dr. David S. Celermajer, Department of Cardiology, Royal Prince Alfred Hospital, Missenden Road, Camperdown NSW 2050, Sydney, Australia
davidc{at}card.rpa.cs.nsw.gov.au
OBJECTIVES
We sought to study the effects of a fatty meal on vascular reactivity, including endothelial function and maximal vasodilation.
BACKGROUND
Recent reports regarding the physiological changes in peripheral vasculature after eating a fatty meal have been controversial.
METHODS
Twelve volunteers were studied before, 3 h after, and 6 h after a high-fat meal (1030 kcal, 61 g fat) rich in saturated fatty acids, and 10 were restudied after a similar meal rich in monounsaturated fatty acids. Endothelial function was assessed as flow-mediated dilatation (FMD) in the brachial artery using ultrasound. Resting and postischemic forearm blood flow (FBF) were recorded using venous occlusion strain-gauge plethysmography, before, and every 10 to 15 s after, 5 min upper arm ischemia.
RESULTS
Brachial artery basal diameter, resting FBF and postischemic hyperemia increased after high-fat meals (all p < 0.001), whereas FMD did not change. The increase in resting FBF correlated with increases in postprandial insulin (r = 0.80, p < 0.002) and triglyceride (r = 0.77, p < 0.005) levels.
CONCLUSIONS
We concluded that eating a fatty meal induces vasodilation and increases resting and stimulated FBF and that these observations are probably mediated by postprandial changes in insulin and/or triglyceride levels. The metabolic changes that occur after meals are not associated with impaired endothelial nitric oxide release in the conduit arteries.
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