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1  nitric oxide-mediated endothelium-dependent vasomotion.
2 rtrophy, arteriolar hypertrophy, and altered vasomotion.
3 nt vasculopathy on myocardial blood flow and vasomotion.
4 dentified a genetic basis for stress-induced vasomotion.
5 LFPs, supporting that these reflect cerebral vasomotion.
6  CSF mobility can be increased by entraining vasomotion.
7  envelope over gamma-band activity, entrains vasomotion.
8  lumen enlargement, and the lack of reactive vasomotion.
9 ement, plaque regression, and restoration of vasomotion.
10            Insulin also increases arteriolar vasomotion.
11 was puzzled by these dramatic alterations in vasomotion.
12 al smooth muscle cells is a prerequisite for vasomotion.
13 , is known to regulate endothelium-dependent vasomotion.
14 striction, relaxation, and the phenomenon of vasomotion.
15 iolar [Ca2+]i oscillations and corresponding vasomotion.
16 osphorylation of this residue is involved in vasomotion.
17 c oxide (NO), improves endothelium-dependent vasomotion.
18 ed blood viscosity and not abnormal coronary vasomotion.
19  possibility of increasing transport through vasomotion.
20 erum triglyceride levels, indicating lack of vasomotion.
21 wo prominent activity patterns emerged: fast vasomotion across the entire hemisphere and slow vasomot
22 namic multiplexed imaging of cerebrovascular vasomotion activity and the single-cell-level neutrophil
23 ions enhanced CSF inflow, demonstrating that vasomotion acts as a pump driving CSF into the brain.
24  The aim of our study was to assess coronary vasomotion after successful revascularization of chronic
25 CSF) through the brain is driven by cerebral vasomotion, along with respiratory and cardiac forces.
26                             Especially brain vasomotion and arterial pulsations modulated by noradren
27 coeruleus induced anti-correlated changes in vasomotion and CSF signal.
28 rials of BVSs report restoration of arterial vasomotion and elimination of serious complications such
29 ceptor inhibition improves abnormal coronary vasomotion and endothelial dysfunction in patients with
30           The cellular mechanisms underlying vasomotion and its physiological role have not been comp
31 e spatiotemporal characteristics of cerebral vasomotion and its relationship to neural activity in an
32           UGABD correctly detected pulsatile vasomotion and measured area within 5% of the true value
33 c oxide (NO), improves endothelium-dependent vasomotion and NO activity in atherosclerosis.
34 , most likely, endothelium-mediated coronary vasomotion and PET-measured MBF further supports the val
35 es in our understanding of the regulation of vasomotion and vascular remodeling that have led to "rev
36  The effect of long-term smoking on coronary vasomotion and vasodilator capacity in healthy smokers i
37  cold pressor testing (endothelium-dependent vasomotion), and during dipyridamole-induced hyperemia i
38  of the artery, allowing cyclic pulsatility, vasomotion, and adaptative remodelling, by unlocking and
39 g the impact on atherosclerosis, thrombosis, vasomotion, and arrhythmogenesis.
40 in activity and, hence, physiologic coronary vasomotion appears to be influenced by serum ACE levels
41            Coronary endothelial function and vasomotion are impaired in smokers without coronary dise
42  these findings indicate that alterations in vasomotion are the primary means by which the CBR regula
43 h arteriole radius and Ca(2+) oscillations, "vasomotion," are damped due to neural induced astrocytic
44 ltrasound, optical coherence tomography, and vasomotion assessment.
45 f area reduction at 6 months and recovery of vasomotion at 1 year.
46 study aimed to compare the in-stent/scaffold vasomotion between MgBRS and permanent metallic sirolimu
47                  Increasing the amplitude of vasomotion by means of visually evoked vascular response
48   The co-primary endpoints of this study are vasomotion (change in mean lumen diameter before and aft
49 1), and displayed less endothelium-dependent vasomotion (% change segmental lumen volume: 2.1 +/- 0.8
50 ly display an oscillatory phenomenon defined vasomotion, consistent with periodic diameter variations
51                                              Vasomotion correlated with paravascular clearance of flu
52                               Improvement in vasomotion correlates most significantly with markers of
53 ysiological tissue myoglobin concentrations, vasomotion did not improve tissue oxygenation.
54 se values calculated from experimental data, vasomotion does inhibit mass transport to tissue in a on
55 n of a foreign body, restriction of vascular vasomotion due to a metal cage, and the risk of late and
56                            Abnormal coronary vasomotion due to endothelial dysfunction contributes to
57                          Abnormal epicardial vasomotion during CPT and exercise also improved with lo
58 is or its risk factors, we measured coronary vasomotion during flow-mediated dilation (FMD) in respon
59 oles or pericyte-covered capillaries control vasomotion during neurovascular coupling remains controv
60 nts with atherosclerosis improves epicardial vasomotion during stress, probably by improving endothel
61  of atherosclerosis, contributes to abnormal vasomotion during stress.
62 dial ischemia by promoting abnormal coronary vasomotion during stress.
63  whether assessment of endothelium-dependent vasomotion (EDV) with brachial artery ultrasound (BAUS)
64 tate blood volume oscillations and decreased vasomotion following the ablation of type-I nNOS neurons
65 e nongenomic effects of steroids, control of vasomotion has received increasing attention.
66 tial in rat isolated cerebral vessels during vasomotion (i.e., rhythmic fluctuations in arterial diam
67 m studies on mouse cortex that modulation of vasomotion, i.e., intrinsic ultra-slow (0.1 Hz) fluctuat
68 Similarly, acetylcholine-mediated epicardial vasomotion improved in segments that initially constrict
69                         We assessed coronary vasomotion in 110 patients (mean [+/- SD] age 56 +/- 10
70  infra-slow oscillation (ISO) is a source of vasomotion in endogenic (E; 0.005-0.02 Hz), neurogenic (
71 n impairment in endothelium-related coronary vasomotion in overweight individuals to an impairment of
72 fixed mice to assess the role of spontaneous vasomotion in paravascular clearance.
73 dial and microvascular endothelium-dependent vasomotion in patients with atherosclerosis or its risk
74                Targeting naturally occurring vasomotion in patients with CAA or AD may be a promising
75 actors were not predictive of stress-induced vasomotion in patients with CAD.
76 ive protein (CRP) serum levels, and coronary vasomotion in patients with coronary risk factors but wi
77  abolished abnormal flow-mediated epicardial vasomotion in patients with endothelial dysfunction, in
78                           (Abnormal Coronary Vasomotion in Patients With Suspected CAD But Normal Cor
79 ells, leading to increased flow velocity and vasomotion in pial and penetrating arterioles.
80               Endothelium-dependent coronary vasomotion in response to acetylcholine (10(-8) to 10(-6
81 nitric oxide-mediated, endothelium-dependent vasomotion in response to cold pressor testing.
82 aline-activated inward current important for vasomotion in these resistance arteries.
83 ether Akt can regulate endothelium-dependent vasomotion in vivo using a rabbit femoral artery model o
84 NOCA have identifiable disorders of coronary vasomotion including microvascular and vasospastic angin
85 importance of the frequency and amplitude of vasomotion-induced blood flow oscillations was studied.
86 ons of hypoxia under steady flow conditions, vasomotion-induced flow oscillations can significantly i
87  (iii) tumor blood flow regulation via local vasomotion; (iv) the hemodynamic response to a systemic
88 ncreased degradation of NO by the blood, and vasomotion-like 0.1-0.3 Hz oscillations could also be ge
89 sponse to cold suggests a defect in coronary vasomotion likely located at the level of the coronary e
90                         Thus, entrainment of vasomotion links neuronal pathways to functional connect
91 d suggest that age-related reduction of this vasomotion may contribute to impaired clearance of Abeta
92  edema, endothelial dysfunction and impaired vasomotion, microembolization of atherothrombotic debris
93 nitric oxide-mediated, endothelium-dependent vasomotion occur with increasing severity of insulin-res
94          However, the possible engagement in vasomotion of cell metabolic oscillations of mitochondri
95  luminal dimensions as a result of recovered vasomotion of the scaffolded vessel.
96  tissue and blood to quantify the effects of vasomotion on mass transport to tissue.
97  was to investigate the effect of arteriolar vasomotion on oxygen transport from capillary networks.
98 d validated index of flow-dependent coronary vasomotion on quantitative angiography.
99        Characteristic baseline low frequency vasomotion oscillations (0.17 Hz) were observed after L-
100 n interaction occurred between L-NNA induced vasomotion oscillations and the AFC response with the gr
101 he effects of other vasodilators involved in vasomotion oscillations and the AFC response.
102 oprotein A-1 titers correlated with improved vasomotion (p = 0.027 and 0.005, respectively).
103   Our results suggest that abnormal coronary vasomotion plays a pathogenic role in this setting and t
104        While changes in peripheral pulse and vasomotion power were significant the changes in pulse r
105 sel wall, thereby preventing normal coronary vasomotion, preclude bypass grafting and can provoke lon
106 ics, measured via the blood volume pulse and vasomotion, provide a valuable way of monitoring physiol
107 However, we speculate that abnormal coronary vasomotion (reduced vasodilatation with exercise = reduc
108 safety and efficacy of this new device, with vasomotion restoration and continued degradation over ti
109                         The process known as vasomotion, rhythmic oscillations in vessel diameter, ha
110 motion across the entire hemisphere and slow vasomotion seen as a travelling wave running through the
111 eral pulse signal power (by 36% +/- 29%) and vasomotion signal power (by 50% +/- 26%) occur during pe
112 sion of the study is that a general model of vasomotion that predicts experimental data can be constr
113 s exhibited Ca2+ and diameter oscillations ("vasomotion") that were rapidly suppressed by ES.
114                          For the endpoint of vasomotion, the comparison was tested using a two-sided
115                                              Vasomotion, the name given to the physiological phenomen
116 The vascular model includes a description of vasomotion, the vascular oscillatory response to transmu
117                                              Vasomotion, vascular oscillations at ~ 0.1 Hz, may serve
118 , our group demonstrated impaired testicular vasomotion via alpha1-adrenergic receptor activation and
119 ffect of myoglobin on oxygen delivery during vasomotion was also examined.
120 onary endothelium-dependent and -independent vasomotion was assessed by intracoronary infusions of ac
121                        Endothelium-dependent vasomotion was assessed early posttransplant in 20 patie
122                                     Coronary vasomotion was assessed in 76 patients (average age 59.9
123                                    Moreover, vasomotion was associated with low tissue oxygen and was
124                No difference in ACH-mediated vasomotion was detected between the three ACE genotypes.
125  (SD 0.37), and angiographically discernable vasomotion was documented in 20 (80%) of 25 patients.
126                                We found that vasomotion was driven by the arterial tree.
127                    Improvement in epicardial vasomotion was most prominent in segments with baseline
128                                 The abnormal vasomotion was not an acute response to the high-fat die
129                                       Higher vasomotion was noticed in testicular blood vessels of ad
130 ared with IS, endothelium-dependent coronary vasomotion was significantly diminished in IR (-56%), as
131       In a subgroup of 14 patients, coronary vasomotion was tested in distal segments: incremental at
132 nd 9 control subjects, endothelium-dependent vasomotion was tested with intracoronary ACH (30 microg/
133             Bradykinin, but not ACH-mediated vasomotion, was depressed in epicardial segments that co
134 cate that heightened sleep pressure promotes vasomotion, whereas slow-wave-rich sleep amplifies respi
135 hanisms underlying endothelium-mediated skin vasomotion, which might be altered in the presence of me
136 illaries, pausing is presumed to result from vasomotion-which has been postulated as necessary for th
137  endothelial cells disrupt normal control of vasomotion, with a reduction of effective nitric oxide a

 
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