ライフサイエンスコーパス: ventricular pressure

1 sure and maximal rate of development of left ventricular pressure).

2 ure product and the first derivative of left ventricular pressure.

3 decreased myocardial contractility and left ventricular pressure.

4 bited TdP, but caused a 15+/-8% drop of left ventricular pressure.

5 onduit obstruction, regurgitation, and right ventricular pressure.

6 pidly in early systole in response to rising ventricular pressure.

7 responsible for observed increases in right ventricular pressures.

8 er dose of verapamil without effects on left ventricular pressure (0.06 mg/kg) was not antiarrhythmic

9 ast, have normal heart function despite left ventricular pressures 25% higher than wild type.

10 On the basis of end-diastolic left ventricular pressure, 34 MI rats were classified as nonf

11 ts transduced with Ad.PL had lower peak left ventricular pressure (58.3 +/- 12.9 mmHg, n = 8) compare

12 ter (30+/-11 ms, P<0.015) and at higher left-ventricular pressure (61+/-9 mm Hg, P<0.001) than in the

13 significantly improved the recovery of left ventricular pressure (73+/-5 versus 51+/-4 mm Hg; P<0.05

14 Left ventricular pressure, action potential duration, and cor

15 ic pressure and a decrease in developed left ventricular pressure (all P<0.01 versus baseline) in the

16 sure and reduced peak and end-diastolic left ventricular pressures (all P<0.05).

17 ne restored CcOX activity and increased left ventricular pressure and +/-dP/dt toward sham values fol

18 Left ventricular pressure and cardiac efficiency improved mor

19 ogs chronically instrumented to measure left ventricular pressure and dimension.

20 Dietary nitrate reduced the right ventricular pressure and hypertrophy, and pulmonary vasc

21 This increased left ventricular pressure and increased pressure development

22 ount of particulate intake, changes in right ventricular pressure and intimal thickening of pulmonary

23 ncreased mean heart rate, peak positive left ventricular pressure and its first time-derivative, and

24 00 ft or Denver altitude for 3 wk, and right ventricular pressure and lung histology were assessed.

25 Left ventricular pressure and maximal change in pressure over

26 od flow and the maximum rate of rise in left ventricular pressure and reduced peak and end-diastolic

27 00 (0.4 and 0.8 mg/kg) had no effect on left ventricular pressure and suppressed dofetilide-induced T

28 We measured the left ventricular pressure and volume continuously with a cond

29 Left ventricular pressure and volume data were determined via

30 Characteristics of left ventricular pressure and volume unloading between these

31 diastolic filling pressures (pre-A wave left ventricular pressure) and Doppler mitral inflow at basel

32 orearm blood flow, coronary blood flow, left ventricular pressure, and cardiac output were made by ve

33 Aortic pressure, electrocardiogram, left ventricular pressure, and left ventricular pressure valu

34 dial CcOX activity, oxygen consumption, left ventricular pressure, and pressure developed during isov

35 e mean pulmonary artery pressure, mean right ventricular pressure, and pulmonary vascular resistance

36 ductions in mean arterial pressure, systolic ventricular pressure, and the absolute values of both po

37 nted to measure aortic, left atrial and left ventricular pressures, and regional myocardial function

38 transporter expression causes elevated right ventricular pressures, and this occurs before the onset

39 overall valve opening-closing dynamics, left ventricular pressure, aortic pressure, blood flow rate,

40 Because BNP reflects both elevated left ventricular pressure as well as neurohormonal modulation

41 ion fraction, analog differentiation of left ventricular pressure at 40 mm Hg, and rate of maximal le

42 ance index, the first derivative of the left ventricular pressure at a left ventricular pressure of 5

43 s in humans an equation relating tau to left ventricular pressure at peak -dP/dt (P0), pressure at mi

44 tes of reperfusion, maintaining CPP and left ventricular pressure at preischemic values.

45 Larger left heart structures and higher left ventricular pressure at the time of intervention were as

46 posomes/copolymer attenuated increased right ventricular pressure by approximately 50% and completely

47 maximum of the first time derivative of left ventricular pressure by dobutamine was blunted by intrap

48 ransesophageal long-axis echocardiograms and ventricular pressure by micromanometer provided end-dias

49 Contrast left ventriculograms, ventricular pressures, cardiac output, isovolumetric rel

50 y (LAD) bypass were instrumented with a left ventricular pressure catheter and 2 subepicardial cylind

51 by using echocardiography and ultraminiature ventricular pressure catheters.

52 High right ventricular pressures caused septal shift as demonstrate

53 t 270 beats per minute, and the rate of left ventricular pressure change (LV dP/dt) was monitored.

54 ea produced minimal changes in systolic left ventricular pressure compared with baseline sinus rhythm

55 time delay between upslopes of LV and right ventricular pressure curves, and systolic function was a

56 exponential time constant of isovolumic left ventricular pressure decay (Tau) and the "stiffness" coe

57 We contrasted various methods for assessing ventricular pressure decay time constants to test whethe

58 pressure of 40 mm Hg (dP/dt40), rate of left ventricular pressure decline (-dP/dt), and a lower left

59 pressure of 40 mm Hg (dP/dt40), rate of left ventricular pressure decline (-dP/dt), and end-tidal PCO

60 essure at 40 mm Hg, and rate of maximal left ventricular pressure decline were continuously measured

61 re of 40 mm Hg, and the maximum rate of left ventricular pressure decline were significantly less imp

62 The rate of left ventricular pressure decrease was unchanged.

63 ive and congenital PA stenoses groups, right ventricular pressure decreased (right ventricular pressu

64 Peak left ventricular pressure decreased after TAVR (186 +/- 36 mm

65 However, large increases in ventricular pressure decreased resistance by only 9+/-2.

66 and then cardiac catheterization, where left ventricular pressure development (+dP/dt) and decline (-

67 icant reduction in the maximum rates of left ventricular pressure development and pressure decline in

68 celeration of cross-bridge kinetics and left ventricular pressure development cannot be achieved in i

69 , fractional shortening and the rate of left ventricular pressure development decreased by 36% and 32

70 a percentage of the zone at risk; ZAR), left ventricular pressure development, and coronary flow were

71 sue and showed electrical conductivity, left ventricular pressure development, and metabolic function

72 e stress, VS attenuated the increase in left ventricular pressure-diameter area from 235.9 +/- 72.8 t

73 cious dogs chronically instrumented for left ventricular pressure-dimension analysis, PDE5A inhibitio

74 astolic pressure (LVEDP), and developed left ventricular pressure (dLVP=LVSP-LVEDP), ischemia-reperfu

75 sumption (MVO(2)), peak rate of rise of left ventricular pressure (dP/dt(max)), stroke work (SW), and

76 ximal values of the first derivative of left ventricular pressure (dP/dt) were significantly improved

77 stress and positive first derivative of left ventricular pressure (dP/dt).

78 sitive and negative first derivative of left ventricular pressure (dP/dt).

79 (LVSP), the maximum first derivative of left ventricular pressure (dp/dtmax ), and the slope of the e

80 mine increased the peak rate of rise of left ventricular pressure (+dP/dt) by 49 +/- 8% (p < 0.001) a

81 evealed no differences in heart weight, left ventricular pressure, dP/dt, cardiac index, time constan

82 Left ventricular pressure, dP/dt40, negative dP/dt and cardia

83 scordance between right ventricular and left ventricular pressures during inspiration, a sign of incr

84 left ventricular pressure rise (+dP/dt) and ventricular pressure fall (-dP/dt).

85 ratory changes in left ventricular and right ventricular pressure for the diagnosis of CP at cardiac

86 ontracture as indicated by increases in left ventricular pressure from 9+/-3 to 33+/-6 mm Hg (p < .05

87 imal weight, mean impact velocity, mean left ventricular pressure generated by the blow, mean QRS dur

88 In multivariable analysis, mean left ventricular pressure generated by the blow, mean QRS dur

89 Peak left ventricular pressure generated by the chest blow was rel

90 CC significantly improves the left and right ventricular pressure-generating capability and, in the s

91 However, ventricular pressures had to increase to 152/18 mmHg (sy

92 eases in heart rate and rate of rise in left ventricular pressure, improvement of regional coronary f

93 These previous studies, however, used left ventricular pressure in formulas that assumed the assume

94 Left ventricular pressures in vivo and cardiomyocyte sarcomer

95 ance vessels, and significantly higher right ventricular pressures in vivo.

96 pulmonary vascular obstruction induced right ventricular pressure increase and dilatation, but left v

97 al function, as measured by the rate of left ventricular pressure increase at 40 mm Hg, left ventricu

98 ignificantly less depression in rate of left ventricular pressure increase measured at a left ventric

99 Left ventricular pressure, rate of left ventricular pressure increase measured at a left ventric

100 lar end-diastolic pressure, the rate of left ventricular pressure increase measured at a left ventric

101 The maximal rate of ventricular pressure increase or decrease (+/-dP/dtmax),

102 f1;O2 did not change with DCC; however, peak ventricular pressure increased substantially, so that th

103 right ventricular pressure decreased (right ventricular pressure indexed to femoral artery pressure

104 Left ventricular pressure is 2-fold higher than wild type, an

105 We demonstrate that left ventricular pressure is closely linked to KATP channel a

106 The AHR (maximum rate of left ventricular pressure [LV-dP/dt(max)]) was assessed at im

107 Left ventricular pressure (LVP) and ECG were monitored during

108 pass grafting, high-fidelity left atrial and ventricular pressure measurements were obtained synchron

109 using Mikro-Tip catheter transducers, right ventricular pressure measurements, and analyses of organ

110 l-anesthetized intact dogs arterial and left ventricular pressure (Millar) and left ventricular volum

111 lation parameters, Pt was calculated as left ventricular pressure minus balloon luminal pressure.

112 Ventricular pressure, monophasic action potential, and s

113 graphy (n = 4 per group), and right and left ventricular pressure (n = 5 and n = 4 per group, respect

114 Significant reductions in left ventricular pressures occurred in vivo and in cardiomyoc

115 The volume intercept at left ventricular pressure of 100 mm Hg increased from 43 +/-

116 end-systolic volume at an end-systolic left ventricular pressure of 100 mm Hg.

117 ation hearts, V(30) (ex vivo volume yielding ventricular pressure of 30 mm Hg) was decreased in the l

118 te of left ventricular pressure rise at left ventricular pressure of 40 mm Hg (dP/dt40) and fall (neg

119 ricular pressure increase measured at a left ventricular pressure of 40 mm Hg (dP/dt40), rate of left

120 ricular pressure increase measured at a left ventricular pressure of 40 mm Hg (dP/dt40), rate of left

121 ricular pressure increase measured at a left ventricular pressure of 40 mm Hg, and the maximum rate o

122 e of the left ventricular pressure at a left ventricular pressure of 50 mm Hg, rate-pressure product,

123 in LVdP/dtmax (maximal rate of rise of left ventricular pressure) of >/=90% of the maximum LVdP/dtma

124 n PA diameter; and 2) 25% reduction in right ventricular pressure or 50% decrease in PA gradient or p

125 cular circulation: 1) 20% reduction in right ventricular pressure or 50% increase in PA diameter; and

126 rt populations: (1) surgically induced right ventricular pressure overload (PO), and (2) sustained tr

127 An adult feline right ventricular pressure overload (RVPO) model was used to e

128 ure is usually due to a combination of right ventricular pressure overload and contractile abnormalit

129 Pulmonary hypertension can lead to right ventricular pressure overload and failure.

130 volved in both the cardiac response to acute ventricular pressure overload and the cardiac hypertroph

131 ylation increased to 23% in response to left ventricular pressure overload as compared with 7% phosph

132 al postnatal cardiac growth, concurrent left ventricular pressure overload hypertrophy did not synerg

133 ular function despite persistent severe left ventricular pressure overload in ascending aortic-banded

134 Left ventricular pressure overload in mouse working hearts pr

135 Right ventricular pressure overload in patients with CTEPH cau

136 e study included wild-type mice subjected to ventricular pressure overload or fasting, as well as pat

137 rdial FAO enzymes was delineated in a murine ventricular pressure overload preparation to characteriz

138 Ventricular pressure overload studies in mice, together

139 data from our lab has shown that, following ventricular pressure overload, GRK5, a primary cardiac G

140 gulator of pathological cardiac growth after ventricular pressure overload, supporting its role as an

141 kinase, promoting an intolerance to in vivo ventricular pressure overload; however, its endogenous r

142 ciation was seen as early as 4 h after right ventricular pressure overloading, increased through 48 h

143 Schistosoma-induced PH, with decreased right ventricular pressures, pulmonary vascular remodeling, an

144 r (LV) inotropic effects (adjusted peak left ventricular pressure rate of rise (dP/dt)max/P, 21.2 +/-

145 Left ventricular pressure, rate of left ventricular pressure

146 ypass, the average intraoperative right/left ventricular pressure ratio was 55% +/- 13%.

147 High-fidelity left atrial and left ventricular pressure recordings with simultaneous Dopple

148 anti-miRs via measurement of systolic right ventricular pressure, right ventricular hypertrophy, and

149 ickening as well as the maximal rate of left ventricular pressure rise (+dP/dt) and ventricular press

150 set of sepsis, the maximal rates of the left ventricular pressure rise (+dP/dtmax) and fall (-dP/dtma

151 P and BiVP (% change in maximal rate of left ventricular pressure rise [LVdP/dtmax]) was measured in

152 ular systolic pressure, maximal rate of left-ventricular pressure rise and decline (+dP/dt, -dP/dt),

153 ickening as well as the maximal rate of left ventricular pressure rise and fall (+dP/dt and -dP/dt).

154 Cardiac index and the rate of left ventricular pressure rise at left ventricular pressure o

155 of key parameters such as arterial and left ventricular pressures, serum lipoprotein, and other biom

156 ith intracardiac transducers to measure left ventricular pressure, sonomicrometer crystals in the lef

157 upports an improvement in cardiac output and ventricular pressures, these favorable hemodynamics may

158 Direct curve fitting to the left ventricular pressure trace by Levenberg-Marquardt regres

159 diogram, left ventricular pressure, and left ventricular pressure value of 40 mm Hg were continually

160 s followed by a terminal measurement of left ventricular pressure volume loops.

161 Ventricular pressure, volume, and function were recorded

162 Left-ventricular pressure-volume analyses in adult homozygous

163 /-) mice, and that the leftward shifted left ventricular pressure-volume curve in the MHCsTNF/c-kit(+

164 catheterization to define Starling and left ventricular pressure-volume curves.

165 ithout significant myocardial necrosis (left ventricular pressure-volume curves; 1% triphenyltetrazol

166 PR was estimated from right ventricular pressure-volume loops generated by conductan

167 ved PR fraction and that obtained from right ventricular pressure-volume loops generated by use of co

168 sal PR fraction derived by MR and from right ventricular pressure-volume loops had a correlation coef

169 se velocity mapping and from real-time right ventricular pressure-volume loops with a conductance cat

170 Left ventricular pressure-volume relations were measured in p

171 ced myocardial dysfunction by improving left ventricular pressure-volume relationship.

172 Ventricular pressure-volume relationships have become we

173 Left ventricular pressure-volume relationships utilizing the

174 Left ventricular pressure-volume relationships were assessed

175 (dobutamine 0.3-10 mug/kg/min) using a left ventricular pressure/volume catheter.

176 e and dobutamine infusions simultaneous with ventricular pressure-volumetry.

177 ally instrumented to measure aortic and left ventricular pressures, wall thickness, and left circumfl

178 n follow-up period of 2.6 +/- 2 years, right ventricular pressure was < 70% systemic in all patients

179 Right ventricular pressure was elevated 3-fold in normoxic 5-H

180 Left ventricular pressure was monitored.

181 natriuretic peptide (BNP) partially reflects ventricular pressure, we hypothesized that BNP levels co

182 inflow velocities, and direct measurement of ventricular pressure, we investigated developmental chan

183 hrome c and cytochrome a/a3 redox state, and ventricular pressure were continuously measured from iso

184 Ventricular pressures were changed by varying inflow and

185 Diastolic ventricular pressures were increased without evidence of

186 ither endotoxin or saline, systemic and left ventricular pressures were measured, and the first deriv

187 gh fidelity measures of left atrial and left ventricular pressures were obtained simultaneously with

188 t model of full thickness scald injury, left ventricular pressures were recorded in vivo followed by

189 maging, the rats were catheterized, and left ventricular pressures were recorded.

190 Ventricular pressures were separated from those in the a

191 stolic pressure, maximum first derivative of ventricular pressure with respect to time (+dP/dt), stro

192 echo Doppler studies, and closed-chest left ventricular pressures with direct left ventricular punct