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1 aseline and after a flow stimulus induced by reactive hyperemia.
2 nt change in brachial artery diameter during reactive hyperemia.
3  maximal metabolic vasodilation accompanying reactive hyperemia.
4 metaboreceptor muscle afferent activation or reactive hyperemia.
5 hen modeling physiological phenomena such as reactive hyperemia.
6 diated dilation (FMD) in response to forearm reactive hyperemia.
7  (FMD) in the brachial artery in response to reactive hyperemia.
8 using laser Doppler fluxmetry in response to reactive hyperemia.
9  arterial stenosis, dipyridamole stress, and reactive hyperemia.
10 sure brachial artery diameter changes during reactive hyperemia.
11 rin, systemic blood pressure, heart rate, or reactive hyperemia.
12 (10.8+/-5.1 versus 6.5+/-7.2 mL/min), during reactive hyperemia (191.4+/-100.7 versus 260.3+/-138.7 m
13     After the initial peak, but during early reactive hyperemia (5 minutes of reperfusion), 1 hour of
14 al contribution of CRP, IL-6, and sICAM-1 to reactive hyperemia above and beyond known risk factors s
15            Coronary flows were compared with reactive hyperemia after 45 s of coronary occlusion.
16 ular resistance (FVR) at baseline and during reactive hyperemia after 5 minutes of forearm ischemia.
17                                         Mean reactive hyperemia after cuff deflation was similar in t
18 e in brachial artery diameter in response to reactive hyperemia and nitroglycerin, respectively.
19 (capillary density during postocclusive peak reactive hyperemia) and during venous occlusion (venous
20 on in response to transient (short period of reactive hyperemia) and sustained (prolonged period of r
21 ured brachial artery flow-mediated dilation, reactive hyperemia, and serum concentrations of C-reacti
22 jects, we studied microvascular responses to reactive hyperemia, angiotensin II, acetylcholine, and s
23                                              Reactive hyperemia as a parameter of endothelial functio
24 r function (flow-mediated dilation [FMD] and reactive hyperemia) assessed at a subsequent examination
25 nd was predicted by BA diameter (p < 0.001), reactive hyperemia blood flow (p < 0.001), high-density
26                                       During reactive hyperemia, blood flow velocity yielded peak vel
27 terone), FMD (N-ANP, PAI-1, CRP, renin), and reactive hyperemia (BNP, PAI-1, CRP, renin, urine albumi
28                     Retinal blood flow had a reactive hyperemia, but choroidal blood flow did not (e.
29 heophylline (8-PT; 5 mg/kg), which decreased reactive hyperemia by an average of 38%.
30 m blood flow was measured at rest and during reactive hyperemia by venous air plethysmography.
31                    During estradiol therapy, reactive hyperemia caused an 11.1+/-1.0% change in brach
32 s significantly increased at rest and during reactive hyperemia compared with controls and patients w
33  percent change in forearm blood flow during reactive hyperemia compared with forearm blood flow at r
34 onses in the brachial artery diameter during reactive hyperemia: controls (13.7 +/- 6.1), relatives (
35      The increases in peak Vo2 and calf peak reactive hyperemia correlated closely (r = 0.61, p < 0.0
36 the ratio of the digital pulse volume during reactive hyperemia divided by that at baseline.
37 the ratio of the digital pulse volume during reactive hyperemia divided by that at rest.
38 ular dysfunction involving both ischemia and reactive hyperemia during tissue reperfusion.
39 o measured brachial artery reactivity during reactive hyperemia (endothelium-dependent dilation) and
40 carotid IMT and brachial artery responses to reactive hyperemia (endothelium-dependent vasodilation)
41                      After short episodes of reactive hyperemia, FMD was abolished by local infusion
42                                              Reactive hyperemia following limb ischemia/occlusion is
43 on during ischemia (SRi) and gradient during reactive hyperemia (Grad).
44 illary recruitment during postocclusive peak reactive hyperemia had an odds ratio for albuminuria of
45 r and dilatation after prolonged episodes of reactive hyperemia, hand warming, and distal infusion of
46 yperemia) and sustained (prolonged period of reactive hyperemia, hand warming, or an incremental infu
47 e in brachial artery diameter in response to reactive hyperemia in adolescents age 13 to 16 years who
48 ivity of the cardiovascular system, enhanced reactive hyperemia in peripheral vascular beds, and symp
49 formed by data regarding skin blood flow and reactive hyperemia in response to pressure, could provid
50                                         Peak reactive hyperemia increased significantly in the calves
51 +0.02+/-0.29, P=0.008) and tended to improve reactive hyperemia index (+0.30+/-0.45 versus -0.17+/-0.
52 at 6 months was associated with increases in reactive hyperemia index (0.38 +/- 0.14, p = 0.009) and
53 ediated vasodilation (beta = 0.1, p = 0.03), reactive hyperemia index (beta = 0.23, p < 0.001), pulse
54  output displayed stronger correlations with reactive hyperemia index (r = -0.63 vs. r = -0.31; Meng
55  (peripheral arterial tonometry) detected by reactive hyperemia index (RHI) and EPCs and CPCs by flow
56 peripheral artery tonometry to determine the reactive hyperemia index (RHI), and microvascular functi
57         Endothelial function was assessed by reactive hyperemia index after upper arm cuff occlusion.
58 ted significant negative correlation between reactive hyperemia index and P2Y12 reaction unit (r=-0.3
59 able logistic regression analysis identified reactive hyperemia index as an independent and significa
60 pheral endothelial function was expressed as reactive hyperemia index using reactive hyperemia periph
61 , fever day, and body mass index, enrollment reactive hyperemia index was associated with a 4-fold in
62 lar nitric oxide bioavailability measured as reactive hyperemia index was significantly higher at enr
63                                              Reactive hyperemia index was significantly lower in high
64               The primary outcome, change in reactive hyperemia index, a validated measurement of end
65 hial flow-mediated dilatation, microvascular reactive hyperemia index, aortic hemodynamics, pulse wav
66 abnormal VR displayed more severely impaired reactive hyperemia index, increased liver stiffness, low
67 nary endothelial function was assessed using reactive hyperemia index.
68 crovascular function was assessed as digital reactive hyperemia index.
69  in 30-second intervals for 4 minutes during reactive hyperemia induced by 5-minute forearm cuff occl
70 ress and endothelial dysfunction assessed by reactive hyperemia-induced flow-mediated dilation (FMD).
71   Endothelial function, measured as ischemic reactive hyperemia (IRH) and related biomarkers, were fo
72            Brachial artery ultrasound during reactive hyperemia is a noninvasive method of assessing
73      These data suggest that the response to reactive hyperemia is attenuated in cardiogenic shock.
74 tion of a brachial artery diameter following reactive hyperemia is measured precisely using ultrasono
75 ing for changes in brachial artery diameter, reactive hyperemia, low-density lipoprotein cholesterol,
76                                         Peak reactive hyperemia (mL.min-1.100 mL-1) was determined in
77                        It is well known that reactive hyperemia occurs following a period of ischemia
78                                              Reactive hyperemia of the bronchial circulation has been
79 ure with age and blood pressure by using the reactive hyperemia optical coherence tomography angiogra
80 flow-mediated vasodilation and microvascular reactive hyperemia (p < 0.05 for all).
81  than individuals without CP (P = 0.03 after reactive hyperemia; P = 0.05 after sublingual nitrate).
82                                              Reactive hyperemia PAT scores following mental stress we
83                 We investigated the value of reactive hyperemia peripheral arterial tonometry (RH-PAT
84  expressed as reactive hyperemia index using reactive hyperemia peripheral arterial tonometry.
85                                              Reactive hyperemia-peripheral arterial tonometry (RH-PAT
86 d NO-dependent endothelial function by using reactive hyperemia-peripheral arterial tonometry (RH-PAT
87                                              Reactive hyperemia produced a time-dependent increase in
88 e percent change in arterial diameter during reactive hyperemia relative to the baseline.
89  correlations of CRP, IL-6, and sICAM-1 with reactive hyperemia remained significant.
90  that retinal blood flow has a postocclusive reactive hyperemia response modulated by occlusion durat
91  ankle-brachial index had (1) a more delayed reactive hyperemia response time, manifesting as an incr
92                                              Reactive hyperemia resulted in 2.7- and 2.3-fold increas
93             Flow-mediated dilation (FMD) and reactive hyperemia (RH) (as measures of macrovascular an
94 investigated by 15-second CAO and subsequent reactive hyperemia (RH) and by the selective intracorona
95                                              Reactive hyperemia (RH) in the forearm circulation is an
96                                         Peak reactive hyperemia significantly increased in the calf b
97 on rates and persistent limb ischemia during reactive hyperemia testing.
98 s of blood flow and oxygen saturation during reactive hyperemia than by conventional static measureme
99  Peak vasodilatation measured in response to reactive hyperemia was 150 times greater in pixel count
100                          Vasodilation during reactive hyperemia was also greater after AT(1) receptor
101                              The response to reactive hyperemia was attenuated in cardiogenic and sep
102 ow-mediated vasodilation in response to peak reactive hyperemia was evaluated in the forearms of 9 pa
103 ood flow at rest, after exercise, and during reactive hyperemia was less in heart failure patients th
104                                           No reactive hyperemia was observed during early reperfusion
105  macrocirculation, a reduced response during reactive hyperemia was observed in the diabetic patients
106                               Post-occlusion reactive hyperemia was observed.
107 ial artery of a healthy volunteer undergoing reactive hyperemia was performed.
108 , collateral blood flow did not increase and reactive hyperemia was robust throughout the occlusion p
109 al microvasculature perfusion in response to reactive hyperemia was significantly lower in high blood
110 thelial function; RH-PAT index, a measure of reactive hyperemia, was calculated as the ratio of the d
111  of EECP therapy; RH-PAT index, a measure of reactive hyperemia, was calculated as the ratio of the d
112                                          For reactive hyperemia, we observed inverse correlations wit
113  RH-PAT, digital pulse volume changes during reactive hyperemia were assessed in 94 patients without
114                Peak Vo2 and calf and forearm reactive hyperemia were measured before and during train
115   Changes in brachial artery diameter during reactive hyperemia were measured by high-resolution ultr
116 iteal arteries and veins during cuff-induced reactive hyperemia with magnetic resonance imaging-based
117                                    There was reactive hyperemia with vascular dilatation and congesti
118 s measured under baseline conditions, during reactive hyperemia (with flow increase causing endotheli
119 l artery diameter at rest and in response to reactive hyperemia (with increased flow causing an endot
120  abnormalities in microvascular responses to reactive hyperemia, with a reduction in area under the c
121 4 cycles of no-flow ischemia with subsequent reactive hyperemia within the femoral region and underwe
122 de synthase within the femoral artery during reactive hyperemia yielded substantial release of nitric

 
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