ライフサイエンスコーパス: reactive hyperemia

1 maximal metabolic vasodilation accompanying reactive hyperemia.

2 metaboreceptor muscle afferent activation or reactive hyperemia.

3 hen modeling physiological phenomena such as reactive hyperemia.

4 diated dilation (FMD) in response to forearm reactive hyperemia.

5 (FMD) in the brachial artery in response to reactive hyperemia.

6 using laser Doppler fluxmetry in response to reactive hyperemia.

7 arterial stenosis, dipyridamole stress, and reactive hyperemia.

8 sure brachial artery diameter changes during reactive hyperemia.

9 rin, systemic blood pressure, heart rate, or reactive hyperemia.

10 aseline and after a flow stimulus induced by reactive hyperemia.

11 nt change in brachial artery diameter during 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 ular resistance (FVR) at baseline and during reactive hyperemia after 5 minutes of forearm ischemia.

16 Mean reactive hyperemia after cuff deflation was similar in t

17 e in brachial artery diameter in response to reactive hyperemia and nitroglycerin, respectively.

18 (capillary density during postocclusive peak reactive hyperemia) and during venous occlusion (venous

19 on in response to transient (short period of reactive hyperemia) and sustained (prolonged period of r

20 ured brachial artery flow-mediated dilation, reactive hyperemia, and serum concentrations of C-reacti

21 jects, we studied microvascular responses to reactive hyperemia, angiotensin II, acetylcholine, and s

22 Reactive hyperemia as a parameter of endothelial functio

23 r function (flow-mediated dilation [FMD] and reactive hyperemia) assessed at a subsequent examination

24 nd was predicted by BA diameter (p < 0.001), reactive hyperemia blood flow (p < 0.001), high-density

25 terone), FMD (N-ANP, PAI-1, CRP, renin), and reactive hyperemia (BNP, PAI-1, CRP, renin, urine albumi

26 Retinal blood flow had a reactive hyperemia, but choroidal blood flow did not (e.

27 heophylline (8-PT; 5 mg/kg), which decreased reactive hyperemia by an average of 38%.

28 m blood flow was measured at rest and during reactive hyperemia by venous air plethysmography.

29 During estradiol therapy, reactive hyperemia caused an 11.1+/-1.0% change in brach

30 s significantly increased at rest and during reactive hyperemia compared with controls and patients w

31 percent change in forearm blood flow during reactive hyperemia compared with forearm blood flow at r

32 onses in the brachial artery diameter during reactive hyperemia: controls (13.7 +/- 6.1), relatives (

33 The increases in peak Vo2 and calf peak reactive hyperemia correlated closely (r = 0.61, p < 0.0

34 the ratio of the digital pulse volume during reactive hyperemia divided by that at baseline.

35 the ratio of the digital pulse volume during reactive hyperemia divided by that at rest.

36 ular dysfunction involving both ischemia and reactive hyperemia during tissue reperfusion.

37 o measured brachial artery reactivity during reactive hyperemia (endothelium-dependent dilation) and

38 carotid IMT and brachial artery responses to reactive hyperemia (endothelium-dependent vasodilation)

39 After short episodes of reactive hyperemia, FMD was abolished by local infusion

40 on during ischemia (SRi) and gradient during reactive hyperemia (Grad).

41 illary recruitment during postocclusive peak reactive hyperemia had an odds ratio for albuminuria of

42 r and dilatation after prolonged episodes of reactive hyperemia, hand warming, and distal infusion of

43 yperemia) and sustained (prolonged period of reactive hyperemia, hand warming, or an incremental infu

44 e in brachial artery diameter in response to reactive hyperemia in adolescents age 13 to 16 years who

45 formed by data regarding skin blood flow and reactive hyperemia in response to pressure, could provid

46 Peak reactive hyperemia increased significantly in the calves

47 +0.02+/-0.29, P=0.008) and tended to improve reactive hyperemia index (+0.30+/-0.45 versus -0.17+/-0.

48 at 6 months was associated with increases in reactive hyperemia index (0.38 +/- 0.14, p = 0.009) and

49 ediated vasodilation (beta = 0.1, p = 0.03), reactive hyperemia index (beta = 0.23, p < 0.001), pulse

50 (peripheral arterial tonometry) detected by reactive hyperemia index (RHI) and EPCs and CPCs by flow

51 peripheral artery tonometry to determine the reactive hyperemia index (RHI), and microvascular functi

52 Endothelial function was assessed by reactive hyperemia index after upper arm cuff occlusion.

53 ted significant negative correlation between reactive hyperemia index and P2Y12 reaction unit (r=-0.3

54 able logistic regression analysis identified reactive hyperemia index as an independent and significa

55 pheral endothelial function was expressed as reactive hyperemia index using reactive hyperemia periph

56 , fever day, and body mass index, enrollment reactive hyperemia index was associated with a 4-fold in

57 lar nitric oxide bioavailability measured as reactive hyperemia index was significantly higher at enr

58 Reactive hyperemia index was significantly lower in high

59 The primary outcome, change in reactive hyperemia index, a validated measurement of end

60 hial flow-mediated dilatation, microvascular reactive hyperemia index, aortic hemodynamics, pulse wav

61 crovascular function was assessed as digital reactive hyperemia index.

62 in 30-second intervals for 4 minutes during reactive hyperemia induced by 5-minute forearm cuff occl

63 ress and endothelial dysfunction assessed by reactive hyperemia-induced flow-mediated dilation (FMD).

64 Endothelial function, measured as ischemic reactive hyperemia (IRH) and related biomarkers, were fo

65 Brachial artery ultrasound during reactive hyperemia is a noninvasive method of assessing

66 These data suggest that the response to reactive hyperemia is attenuated in cardiogenic shock.

67 ing for changes in brachial artery diameter, reactive hyperemia, low-density lipoprotein cholesterol,

68 Peak reactive hyperemia (mL.min-1.100 mL-1) was determined in

69 It is well known that reactive hyperemia occurs following a period of ischemia

70 Reactive hyperemia of the bronchial circulation has been

71 flow-mediated vasodilation and microvascular reactive hyperemia (p < 0.05 for all).

72 than individuals without CP (P = 0.03 after reactive hyperemia; P = 0.05 after sublingual nitrate).

73 Reactive hyperemia PAT scores following mental stress we

74 We investigated the value of reactive hyperemia peripheral arterial tonometry (RH-PAT

75 expressed as reactive hyperemia index using reactive hyperemia peripheral arterial tonometry.

76 d NO-dependent endothelial function by using reactive hyperemia-peripheral arterial tonometry (RH-PAT

77 Reactive hyperemia-peripheral arterial tonometry (RH-PAT

78 Reactive hyperemia produced a time-dependent increase in

79 e percent change in arterial diameter during reactive hyperemia relative to the baseline.

80 correlations of CRP, IL-6, and sICAM-1 with reactive hyperemia remained significant.

81 that retinal blood flow has a postocclusive reactive hyperemia response modulated by occlusion durat

82 ankle-brachial index had (1) a more delayed reactive hyperemia response time, manifesting as an incr

83 Reactive hyperemia resulted in 2.7- and 2.3-fold increas

84 investigated by 15-second CAO and subsequent reactive hyperemia (RH) and by the selective intracorona

85 Reactive hyperemia (RH) in the forearm circulation is an

86 Peak reactive hyperemia significantly increased in the calf b

87 s of blood flow and oxygen saturation during reactive hyperemia than by conventional static measureme

88 Peak vasodilatation measured in response to reactive hyperemia was 150 times greater in pixel count

89 Vasodilation during reactive hyperemia was also greater after AT(1) receptor

90 The response to reactive hyperemia was attenuated in cardiogenic and sep

91 ow-mediated vasodilation in response to peak reactive hyperemia was evaluated in the forearms of 9 pa

92 ood flow at rest, after exercise, and during reactive hyperemia was less in heart failure patients th

93 No reactive hyperemia was observed during early reperfusion

94 macrocirculation, a reduced response during reactive hyperemia was observed in the diabetic patients

95 Post-occlusion reactive hyperemia was observed.

96 ial artery of a healthy volunteer undergoing reactive hyperemia was performed.

97 , collateral blood flow did not increase and reactive hyperemia was robust throughout the occlusion p

98 thelial function; RH-PAT index, a measure of reactive hyperemia, was calculated as the ratio of the d

99 of EECP therapy; RH-PAT index, a measure of reactive hyperemia, was calculated as the ratio of the d

100 For reactive hyperemia, we observed inverse correlations wit

101 RH-PAT, digital pulse volume changes during reactive hyperemia were assessed in 94 patients without

102 Peak Vo2 and calf and forearm reactive hyperemia were measured before and during train

103 Changes in brachial artery diameter during reactive hyperemia were measured by high-resolution ultr

104 iteal arteries and veins during cuff-induced reactive hyperemia with magnetic resonance imaging-based

105 There was reactive hyperemia with vascular dilatation and congesti

106 s measured under baseline conditions, during reactive hyperemia (with flow increase causing endotheli

107 l artery diameter at rest and in response to reactive hyperemia (with increased flow causing an endot

108 abnormalities in microvascular responses to reactive hyperemia, with a reduction in area under the c

109 4 cycles of no-flow ischemia with subsequent reactive hyperemia within the femoral region and underwe

110 de synthase within the femoral artery during reactive hyperemia yielded substantial release of nitric