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1 elax smooth muscle cells in a process termed flow-mediated dilatation.
2 Endothelial function was assessed by flow-mediated dilatation.
3 renergic blockade resulted in an increase in flow-mediated dilatation.
4 ype mice, CHF markedly impaired NO-dependent flow-mediated dilatation.
5 P=0.27), but did ameliorate the reduction in flow-mediated dilatation (0 hours, 4.0+/-1.0; 2 hours, 3
6 0 days after therapy (absolute difference in flow-mediated dilatation, 0.9%; 95% CI, 0.1 to 1.7; P=0.
8 ature was investigated using brachial artery flow-mediated dilatation and carotid artery intima-media
10 there was no consistent relationship between flow-mediated dilatation and free oxidized homocysteine,
11 stiffness), brachial artery reactivity (both flow-mediated dilatation and sublingual glycerol trinitr
12 diameter of the brachial artery during flow (flow-mediated dilatation), and inflammatory biomarkers a
13 ne artery pulsatility index, brachial artery flow-mediated dilatation, and serum concentrations of pl
14 fy endothelial function (via brachial artery flow-mediated dilatation) at sea level (344 m) and high
15 fy endothelial function (via brachial artery flow-mediated dilatation) at sea level (344 m) and high
16 (by 39.7+/-11.8%; P=0.02) but also inhibited flow-mediated dilatation by approximately 80% (P<0.01).
17 In both loading studies, peak reduction in flow-mediated dilatation coincided with maximal reduced
18 n improved endothelial function (measured as flow-mediated dilatation) compared with placebo (dark ch
21 ved arterial dilatation Deltabrachial artery flow-mediated dilatation/Deltadilation response to glyce
24 hours, 31.2+/-3.1 micromol/l, P<0.001), and flow-mediated dilatation fell (0 hours, 4.3+/-0.7; 2 hou
26 on and structure, we examined conduit artery flow mediated dilatation (FMD), an index of nitric oxide
28 tion, there was a significant improvement in flow-mediated dilatation (FMD) (endothelial-dependent di
29 al endothelial function as assessed by using flow-mediated dilatation (FMD) and arterial compliance a
30 chial artery diameter, endothelial-dependent flow-mediated dilatation (FMD) and endothelial-independe
34 imary and secondary outcomes were changes in flow-mediated dilatation (FMD) of the brachial artery, a
38 thelial function assessed by brachial artery flow-mediated dilatation (FMD) was measured before, imme
40 a-3) PUFAs on vascular function measured via flow-mediated dilatation (FMD), laser Doppler iontophore
48 Endothelium-dependent (hyperemia-induced flow-mediated dilatation [FMD]) and -independent (glycer
51 een changes in HDL-induced NO production and flow-mediated dilatation improvement by ET was evident.
58 hypertensive patients exhibited a decreased flow-mediated dilatation in response to postischemic hyp
60 rations > 15-fold in all groups and restored flow-mediated dilatation in the sedentary older men (to
61 l arteries, carotid arteries and aortae, and flow-mediated dilatations in third-order mesenteric resi
62 ontrol subjects during endothelium-dependent flow-mediated dilatation induced by hand skin heating.
63 ement therapy on inflammatory markers and on flow-mediated dilatation is largely beneficial, although
64 s largely beneficial, although the effect on flow-mediated dilatation is modulated according to endot
69 econdary end points of endothelial function (flow-mediated dilatation of the brachial artery) and car
72 d not significantly affect the percentage of flow-mediated dilatation or other measures of vascular f
75 r n-6 PUFAs did not affect the percentage of flow-mediated dilatation (primary endpoint) or other mea
76 biomarker and vascular function measured as flow-mediated dilatation (R = -0.3, P < 0.01) or endothe
77 tral water immersion, heat therapy increased flow-mediated dilatation, reduced arterial stiffness, re
96 dentary human ageing and the preservation of flow-mediated dilatation with physically active ageing.
97 the impairment in peripheral conduit artery flow-mediated dilatation with sedentary human ageing and
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