ライフサイエンスコーパス: vasomotion

1 Insulin also increases arteriolar vasomotion.

2 was puzzled by these dramatic alterations in vasomotion.

3 envelope over gamma-band activity, entrains vasomotion.

4 al smooth muscle cells is a prerequisite for vasomotion.

5 lumen enlargement, and the lack of reactive vasomotion.

6 , is known to regulate endothelium-dependent vasomotion.

7 striction, relaxation, and the phenomenon of vasomotion.

8 iolar [Ca2+]i oscillations and corresponding vasomotion.

9 osphorylation of this residue is involved in vasomotion.

10 ement, plaque regression, and restoration of vasomotion.

11 c oxide (NO), improves endothelium-dependent vasomotion.

12 ed blood viscosity and not abnormal coronary vasomotion.

13 possibility of increasing transport through vasomotion.

14 erum triglyceride levels, indicating lack of vasomotion.

15 nitric oxide-mediated endothelium-dependent vasomotion.

16 rtrophy, arteriolar hypertrophy, and altered vasomotion.

17 nt vasculopathy on myocardial blood flow and vasomotion.

18 The aim of our study was to assess coronary vasomotion after successful revascularization of chronic

19 rials of BVSs report restoration of arterial vasomotion and elimination of serious complications such

20 ceptor inhibition improves abnormal coronary vasomotion and endothelial dysfunction in patients with

21 UGABD correctly detected pulsatile vasomotion and measured area within 5% of the true value

22 c oxide (NO), improves endothelium-dependent vasomotion and NO activity in atherosclerosis.

23 , most likely, endothelium-mediated coronary vasomotion and PET-measured MBF further supports the val

24 es in our understanding of the regulation of vasomotion and vascular remodeling that have led to "rev

25 The effect of long-term smoking on coronary vasomotion and vasodilator capacity in healthy smokers i

26 cold pressor testing (endothelium-dependent vasomotion), and during dipyridamole-induced hyperemia i

27 g the impact on atherosclerosis, thrombosis, vasomotion, and arrhythmogenesis.

28 in activity and, hence, physiologic coronary vasomotion appears to be influenced by serum ACE levels

29 Coronary endothelial function and vasomotion are impaired in smokers without coronary dise

30 these findings indicate that alterations in vasomotion are the primary means by which the CBR regula

31 h arteriole radius and Ca(2+) oscillations, "vasomotion," are damped due to neural induced astrocytic

32 ltrasound, optical coherence tomography, and vasomotion assessment.

33 f area reduction at 6 months and recovery of vasomotion at 1 year.

34 The co-primary endpoints of this study are vasomotion (change in mean lumen diameter before and aft

35 1), and displayed less endothelium-dependent vasomotion (% change segmental lumen volume: 2.1 +/- 0.8

36 Improvement in vasomotion correlates most significantly with markers of

37 ysiological tissue myoglobin concentrations, vasomotion did not improve tissue oxygenation.

38 se values calculated from experimental data, vasomotion does inhibit mass transport to tissue in a on

39 n of a foreign body, restriction of vascular vasomotion due to a metal cage, and the risk of late and

40 Abnormal coronary vasomotion due to endothelial dysfunction contributes to

41 Abnormal epicardial vasomotion during CPT and exercise also improved with lo

42 is or its risk factors, we measured coronary vasomotion during flow-mediated dilation (FMD) in respon

43 oles or pericyte-covered capillaries control vasomotion during neurovascular coupling remains controv

44 nts with atherosclerosis improves epicardial vasomotion during stress, probably by improving endothel

45 of atherosclerosis, contributes to abnormal vasomotion during stress.

46 dial ischemia by promoting abnormal coronary vasomotion during stress.

47 whether assessment of endothelium-dependent vasomotion (EDV) with brachial artery ultrasound (BAUS)

48 e nongenomic effects of steroids, control of vasomotion has received increasing attention.

49 tial in rat isolated cerebral vessels during vasomotion (i.e., rhythmic fluctuations in arterial diam

50 m studies on mouse cortex that modulation of vasomotion, i.e., intrinsic ultra-slow (0.1 Hz) fluctuat

51 Similarly, acetylcholine-mediated epicardial vasomotion improved in segments that initially constrict

52 We assessed coronary vasomotion in 110 patients (mean [+/- SD] age 56 +/- 10

53 n impairment in endothelium-related coronary vasomotion in overweight individuals to an impairment of

54 dial and microvascular endothelium-dependent vasomotion in patients with atherosclerosis or its risk

55 actors were not predictive of stress-induced vasomotion in patients with CAD.

56 ive protein (CRP) serum levels, and coronary vasomotion in patients with coronary risk factors but wi

57 abolished abnormal flow-mediated epicardial vasomotion in patients with endothelial dysfunction, in

58 (Abnormal Coronary Vasomotion in Patients With Suspected CAD But Normal Cor

59 Endothelium-dependent coronary vasomotion in response to acetylcholine (10(-8) to 10(-6

60 nitric oxide-mediated, endothelium-dependent vasomotion in response to cold pressor testing.

61 aline-activated inward current important for vasomotion in these resistance arteries.

62 ether Akt can regulate endothelium-dependent vasomotion in vivo using a rabbit femoral artery model o

63 importance of the frequency and amplitude of vasomotion-induced blood flow oscillations was studied.

64 ons of hypoxia under steady flow conditions, vasomotion-induced flow oscillations can significantly i

65 sponse to cold suggests a defect in coronary vasomotion likely located at the level of the coronary e

66 Thus, entrainment of vasomotion links neuronal pathways to functional connect

67 edema, endothelial dysfunction and impaired vasomotion, microembolization of atherothrombotic debris

68 nitric oxide-mediated, endothelium-dependent vasomotion occur with increasing severity of insulin-res

69 luminal dimensions as a result of recovered vasomotion of the scaffolded vessel.

70 tissue and blood to quantify the effects of vasomotion on mass transport to tissue.

71 was to investigate the effect of arteriolar vasomotion on oxygen transport from capillary networks.

72 d validated index of flow-dependent coronary vasomotion on quantitative angiography.

73 Characteristic baseline low frequency vasomotion oscillations (0.17 Hz) were observed after L-

74 n interaction occurred between L-NNA induced vasomotion oscillations and the AFC response with the gr

75 he effects of other vasodilators involved in vasomotion oscillations and the AFC response.

76 oprotein A-1 titers correlated with improved vasomotion (p = 0.027 and 0.005, respectively).

77 Our results suggest that abnormal coronary vasomotion plays a pathogenic role in this setting and t

78 However, we speculate that abnormal coronary vasomotion (reduced vasodilatation with exercise = reduc

79 safety and efficacy of this new device, with vasomotion restoration and continued degradation over ti

80 The process known as vasomotion, rhythmic oscillations in vessel diameter, ha

81 sion of the study is that a general model of vasomotion that predicts experimental data can be constr

82 s exhibited Ca2+ and diameter oscillations ("vasomotion") that were rapidly suppressed by ES.

83 For the endpoint of vasomotion, the comparison was tested using a two-sided

84 Vasomotion, the name given to the physiological phenomen

85 The vascular model includes a description of vasomotion, the vascular oscillatory response to transmu

86 ffect of myoglobin on oxygen delivery during vasomotion was also examined.

87 onary endothelium-dependent and -independent vasomotion was assessed by intracoronary infusions of ac

88 Endothelium-dependent vasomotion was assessed early posttransplant in 20 patie

89 Coronary vasomotion was assessed in 76 patients (average age 59.9

90 No difference in ACH-mediated vasomotion was detected between the three ACE genotypes.

91 (SD 0.37), and angiographically discernable vasomotion was documented in 20 (80%) of 25 patients.

92 Improvement in epicardial vasomotion was most prominent in segments with baseline

93 The abnormal vasomotion was not an acute response to the high-fat die

94 ared with IS, endothelium-dependent coronary vasomotion was significantly diminished in IR (-56%), as

95 In a subgroup of 14 patients, coronary vasomotion was tested in distal segments: incremental at

96 nd 9 control subjects, endothelium-dependent vasomotion was tested with intracoronary ACH (30 microg/

97 Bradykinin, but not ACH-mediated vasomotion, was depressed in epicardial segments that co

98 illaries, pausing is presumed to result from vasomotion-which has been postulated as necessary for th

99 endothelial cells disrupt normal control of vasomotion, with a reduction of effective nitric oxide a