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 I, 2.2-0.9] Wood units) and transmural right ventricular pressure (10 [95% CI, 15-6] mm Hg) during ex

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

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

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

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

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

15 Left ventricular pressure, action potential duration, and cor

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

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

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

19 Left ventricular pressure and cardiac efficiency improved mor

20 n more severe PH measured by increased right ventricular pressure and decreased pulmonary artery acce

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

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

23 This increased left ventricular pressure and increased pressure development

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

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

26 00 ft or Denver altitude for 3 wk, and right ventricular pressure and lung histology were assessed.

27 aline-treated rats developed increased right ventricular pressure and mass, along with right atrial (

28 Left ventricular pressure and maximal change in pressure over

29 Drug treatment also decreased right ventricular pressure and mitigated pulmonary hypertensio

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

31 00 (0.4 and 0.8 mg/kg) had no effect on left ventricular pressure and suppressed dofetilide-induced T

32 h Ppl demonstrated unchanged transmural left ventricular pressure and systemic blood pressure after t

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

34 Left ventricular pressure and volume data were determined via

35 ion by mapping the relationship between left ventricular pressure and volume throughout the cardiac c

36 Characteristics of left ventricular pressure and volume unloading between these

37 evated P(PL) on hemodynamics, left and right ventricular pressures and pulmonary vascular resistance.

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

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

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

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

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

43 elevated Ppl on hemodynamics, left and right ventricular pressure, and pulmonary vascular resistance.

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

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

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

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

48 regional myocardial work was estimated using ventricular pressure as a surrogate for myocardial stres

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

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

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

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

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

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

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

56 ms to achieve complete repair with low right ventricular pressure by completely incorporating blood s

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

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

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

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

61 A left ventricular pressure catheter and continuous ECGs were u

62 by using echocardiography and ultraminiature ventricular pressure catheters.

63 High right ventricular pressures caused septal shift as demonstrate

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

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

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

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

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

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

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

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

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

73 The rate of left ventricular pressure decrease was unchanged.

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

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

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

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

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

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

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

81 f cardiac myosin, and reduces force and left ventricular pressure development in isolated myofilament

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

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

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

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

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

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

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

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

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

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

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

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

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

95 ar wall, and its surrounding tissues at peak ventricular pressure during the hemodynamic cycle.

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

97 Age-dependent right ventricular pressure elevation, dilation and reduced car

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

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

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

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

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

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

104 neuromodulates the heart and increases left ventricular pressure generating capacity.

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

106 that a single-session of AIH increased left ventricular pressure generation and arterial blood press

107 us increased leaflet surface area exposed to ventricular pressure gradients (ie, billowing leaflets)

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

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

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

111 Left ventricular pressures in vivo and cardiomyocyte sarcomer

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

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

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

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

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

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

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

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

120 on administration of NA, heart rate and left ventricular pressure increased, and activation recovery

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

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

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

124 Passive ventricular pressure-loading experiments further reveal

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

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

127 In Cohort 2, we assessed left ventricular pressure (LVP) during stimulation and recove

128 amic testing to determine the change in left ventricular pressure maximal first derivative (LV dP/dt(

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

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

131 the human disease, including increased right ventricular pressures, medial thickening, neointimal les

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

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

134 Ventricular pressure, monophasic action potential, and s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

150 ities, such as hypertension, leading to left ventricular pressure overload and adverse remodeling of

151 al models of aortic stenosis can induce left ventricular pressure overload and coarsely control the s

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

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

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

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

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

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

158 Left ventricular pressure overload in mouse working hearts pr

159 Right ventricular pressure overload in patients with CTEPH cau

160 We induced persistent left ventricular pressure overload in rats by ascending aorti

161 c fibroblast cell cycle and fibrosis in left ventricular pressure overload induced by transaortic con

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

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

164 Transient activation of AMPK preceding left ventricular pressure overload reduces adverse remodeling

165 Ventricular pressure overload studies in mice, together

166 A prolonged state of left ventricular pressure overload, commonly caused by hypert

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

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

169 ved cardiac dysfunction in animals with left ventricular pressure overload.

170 ns the timing and extent of fibrosis in left ventricular pressure overload.

171 dative stress in response to persistent left ventricular pressure overload.

172 cipitated a robust fibrotic response to left ventricular pressure overload.

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

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

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

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

177 Left ventricular pressure, rate of left ventricular pressure

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

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

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

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

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

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

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

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

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

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

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

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

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

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

192 t of FGFR activation and inhibition on right ventricular pressure, vascular remodeling, and endotheli

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

194 Ventricular pressure, volume, and function were recorded

195 Right ventricular pressure-volume (PV) analysis characterizes

196 Left ventricular pressure-volume (PV) loop measurement provid

197 Left-ventricular pressure-volume analyses in adult homozygous

198 anical function was characterized using left ventricular pressure-volume compliance measurements.

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

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

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

202 , and Wistar-Kyoto rats (n=9) underwent left ventricular pressure-volume loop evaluation and synchron

203 cular function in the form of right and left ventricular pressure-volume loops and ventricular power,

204 Cardiac function was assessed with left ventricular pressure-volume loops during implantation, a

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

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

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

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

209 Left ventricular pressure-volume relations were measured in p

210 The ventricular pressure-volume relationship and time-varyin

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

212 howed inconsistent trends during recovery in ventricular pressure-volume relationships and power outp

213 Ventricular pressure-volume relationships have become we

214 Left ventricular pressure-volume relationships utilizing the

215 Left ventricular pressure-volume relationships were assessed

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

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

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

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

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

221 Left ventricular pressure was monitored.

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

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

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

225 Ventricular pressures were changed by varying inflow and

226 Diastolic ventricular pressures were increased without evidence of

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

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

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

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

231 Ventricular pressures were separated from those in the a

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

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