ライフサイエンスコーパス: aortic pressure

1 AVMs in major organs to explain the reduced aortic pressure.

2 of administration of potent vasodilators on aortic pressure.

3 yperaemia, or with hyperaemia plus increased aortic pressure.

4 raemia, and during hyperaemia plus increased aortic pressure.

5 and ascending aortic rupture with increased aortic pressure.

6 infusion to induce a progressive increase in aortic pressure.

7 sponse to pressure overload without reducing aortic pressure.

8 pecific Nox4 knockout mice exhibited similar aortic pressures.

9 hifted the pressure-response curve to higher aortic pressures.

10 r - 3.4 to 124.0 + or - 6.7 mm Hg), and mean aortic pressure (111 + or - 3.1 to 98 + or - 4.3 mm Hg)

11 istance (22 +/- 13% vs. 24 +/- 11%, p = NS), aortic pressure (2 +/- 9% vs. 0 +/- 6%, p = NS) and pulm

12 2 versus 39.1 +/- 9.0 mm Hg, P = 0.13), mean aortic pressures (30.9 +/- 5.8 versus 28.1 +/- 8.1 mm Hg

13 to limit the reduction in stroke volume when aortic pressure (afterload) is elevated.

14 iac outputs of 5.9 liters per minute against aortic pressure and 7.6 liters per minute against pulmon

15 gh-fidelity catheter recordings of ascending aortic pressure and blood flow velocity at rest and with

16 Aortic pressure and coronary perfusion pressure with HB-

17 ferences in aging on in vivo measurements of aortic pressure and diameter and on extracellular matrix

18 Aortic pressure and flow were measured simultaneously us

19 We measured proximal aortic pressure and flow, forward pressure wave amplitud

20 se wave analysis were used to derive central aortic pressure and hemodynamic indices at baseline and

21 creased arterial stiffness, augments central aortic pressure and increases left ventricular (LV) afte

22 ntaneous wave-free ratio and distal pressure/aortic pressure and not significantly affected by contra

23 Aortic pressures and dimensions in seven dogs were deter

24 se wave analysis were used to derive central aortic pressures and hemodynamic indexes on repeated vis

25 se-wave analysis were used to derive central aortic pressures and hemodynamic indices at repeated vis

26 e substantially different effects on central aortic pressures and hemodynamics despite a similar impa

27 om a beneficial effect of statins on central aortic pressures and hemodynamics.

28 erindopril-based therapy) on derived central aortic pressures and hemodynamics.

29 Left ventricular and aortic pressures and linear flow velocity were measured

30 rugs could have different effects on central aortic pressures and thus cardiovascular outcome despite

31 Central aortic pressures and waveform convey important informati

32 Basal heart rate, aortic pressure, and ejection fraction were comparable i

33 f coronary blood flow (CBF), ventricular and aortic pressure, and ventricular diameter, with catheter

34 er intra-arrest coronary perfusion pressure, aortic pressures, and brain tissue oxygenation.

35 classical semi-spherical vortex model and an aortic pressure-area compliance constitutive relationshi

36 stantaneous wave-free ratio, distal pressure/aortic pressure at rest, and FFR were measured in 763 pa

37 A 33% decline in aortic pressure augmentation in Ex2 (P<0.0001) coincided

38 Consideration of wave reflection and aortic pressure augmentation may explain the lack of ris

39 luded blood lipids, blood pressure, central (aortic) pressure, augmentation index, blood glucose, end

40 closing dynamics, left ventricular pressure, aortic pressure, blood flow rate, and aortic orifice are

41 coronary occlusive pressure divided by mean aortic pressure both subtracted by mean central venous p

42 coronary occlusive pressure divided by mean aortic pressure, both subtracted by central venous press

43 These agents also increased mean aortic pressure but did not alter the pressure gradient

44 with a significant 35% increase in diastolic aortic pressure by 16 mm Hg ([95% CI, 7-25] P=0.0056), 3

45 Invasive central aortic pressure by micromanometer and radial pressure by

46 Central aortic pressures can be accurately estimated from radial

47 entral augmentation index (CAI), and central aortic pressure (CAP).

48 Mean aortic pressure, cardiac output, total blood loss, and t

49 fluid-filled catheter with transformation to aortic pressure, central hemodynamics were measured usin

50 Aortic pressures, central venous pressures, and heart ra

51 occlusive pressure-central venous pressure)/(aortic pressure-central venous pressure); pressure value

52 Atorvastatin did not influence central aortic pressures (change in aortic systolic blood pressu

53 c catheterization to measure ventricular and aortic pressure, coronary blood flow, arterial-coronary

54 Aortic pressure-dimension (chamber) stiffness constants

55 week 8) with LV pressure-volume analysis and aortic pressure-dimension and pressure-flow assessment o

56 s were observed in 10% of vessels because of aortic pressure distortion and in 21% because of distal

57 atio of resting distal coronary pressure and aortic pressure during the complete duration of diastole

58 dual-sensor micromanometer to measure LV and aortic pressures during sinus rhythm and LV free-wall pa

59 Similar to changes in aortic pressure, EECP resulted in a dramatic increase in

60 Aortic pressure, electrocardiogram, left ventricular pre

61 Both were associated with increases in aortic pressure from 20 +/- 3 to 33 +/- 8 mm Hg (p <.001

62 nitro-L-arginine methyl ester increased mean aortic pressure from a mean +/- SEM of 92 +/- 4 to 114 +

63 body surface area <=0.6 cm(2)/m(2) and mean aortic pressure gradient <40 mm Hg) and preserved left v

64 Residual mean aortic pressure gradient (11.6 +/- 4.9 vs. 10.9 +/- 4.9,

65 When exercise-induced changes in mean aortic pressure gradient were added to the multivariable

66 Mean aortic pressure improved from postinfarction levels but

67 1alpha mRNA related in the left ventricle to aortic pressure, in the left atrium to left atrial press

68 In 10 animals, aortic pressure increased from 52 mmHg +/- 24 before thr

69 At baseline and then during EECP, central aortic pressure, intracoronary pressure, and intracorona

70 rtensive" efficacy (failure to lower central aortic pressure), lack of effect on regression of target

71 These effects were preceded by increased aortic pressure (Langendorff constant flow) or decreased

72 luation) study showed less effective central aortic pressure lowering with atenolol-based therapy ver

73 linical outcomes, and differences in central aortic pressures may be a potential mechanism to explain

74 ac arrest in this study was defined by intra-aortic pressure monitoring that is not feasible in clini

75 rest and catheter-based measurements of mean aortic pressure (n=99).

76 turn of spontaneous circulation with an mean aortic pressure of 60 mm Hg (8.0 kPa) after intra-aortic

77 pontaneous circulation with a sustained mean aortic pressure of 60 mm Hg (8.0 kPa) was achieved in si

78 eturn of spontaneous circulation with a mean aortic pressure of 60 mm Hg (8.0 kPa) was achieved.

79 on rates were impaired without any change in aortic pressure or ventricular hypertrophy.

80 .002), but had no effect on heart rate, mean aortic pressure, or right atrial pressure.

81 nvasive arterial pressure waveforms, central aortic pressure, outflow conduit pressure gradient, and

82 eart failure (HF) are apparent using a trans-aortic pressure overload (TAC) model.

83 l cardiac structure and function, but during aortic pressure overload, these mice display rapid onset

84 cardium, epinephrine significantly increased aortic pressure (p < .05) and improved defibrillation ra

85 0.001), cardiac output (p = 0.044), and mean aortic pressure (p < 0.001).

86 Significant reductions in afterload (aortic pressure, P=0.030) and myocardial oxygen demand w

87 distal coronary pressure (Pd) above proximal aortic pressure (Pa) during the early expansion period a

88 tio of distal coronary pressure (Pd) to mean aortic pressure (Pa), and fractional flow reserve (FFR)

89 lar resistance (PVRI) without affecting mean aortic pressure (Pao) or indexed systemic vascular resis

90 Aortic pressure pulsatility significantly decreased in s

91 Distal coronary to aortic pressure ratio (Pd/Pa) and instantaneous wave-fre

92 reserve (FFR) and resting distal coronary to aortic pressure ratio (Pd/Pa) in all patients of the Com

93 FR), and resting distal coronary pressure to aortic pressure ratio (Pd/Pa) were measured in patients

94 The median right ventricle:aortic pressure ratio after repair was 0.35.

95 e ratio (resting distal coronary pressure to aortic pressure ratio and diastolic pressure ratio) and

96 The right ventricular/aortic pressure ratio decreased from 0.6 +/- 0.2 to 0.4

97 The median RV:aortic pressure ratio decreased from 1.0 at baseline to

98 At the initial PA intervention, median RV:aortic pressure ratio decreased from 1.00 to 0.88 (media

99 Patients with a higher preintervention RV:aortic pressure ratio had a greater reduction (P<0.001).

100 r center, with a median right ventricular to aortic pressure ratio of 0.34 (25th, 75th percentiles: 0

101 lts were resting distal coronary pressure to aortic pressure ratio of 0.95+/-0.04, the diastolic pres

102 of Fallot, Genesis stent, higher prestent RV:aortic pressure ratio, and stent malposition associated

103 on and surgical relief in selected cases, RV:aortic pressure ratios decrease substantially and most p

104 hanism accounting for less effective central aortic pressure reduction per unit change in brachial pr

105 heter and re-equalization of distal pressure/aortic pressure, respectively.

106 rimental measurements included instantaneous aortic pressure (subclavian pulse tracings) and flow (ao

107 brachial artery pressure as a surrogate for aortic pressure--the pressure the heart sees.

108 inflow and left atrial pressures, ascending aortic pressure, thermodilution cardiac output and Doppl

109 Correlation with invasive hemodynamic aortic pressure tracings was performed.

110 Central aortic pressure was measured, stored to computer memory,

111 essel using a dual sensor wire while central aortic pressure was recorded using a second wire.

112 Mean aortic pressure was similar between groups.

113 with improvement on therapy displayed higher aortic pressure wave pulsatility (central pulse pressure

114 Increased aortic pressure wave pulsatility and greater decrease in

115 rterial stiffness derived from the ascending aortic pressure waveform.

116 ecorded by applanation tonometry and central aortic pressure waveforms generated using a mathematical

117 Aortic pressure waveforms were derived from a generalize

118 Decreases in aortic pressure were produced at baseline and after nitr

119 onary pressure and flow velocity and central aortic pressure were recorded with sensor wires.

120 Carotid and aortic pressures were also controlled and vascular resis

121 quently, drug-related differences in central aortic pressures were markedly attenuated after adjustme

122 -week recovery, ECG and left ventricular and aortic pressures were recorded in conscious, sedated ani

123 elayed in AS, consistent with a delayed peak aortic pressure, which was partially restored after TAVI

124 We simultaneously measured dorsal aortic pressure with a servonull system and flow velocit

125 there were substantial reductions in central aortic pressures with the amlodipine regimen (central ao