ライフサイエンスコーパス: pulmonary vascular resistance

1 gh cardiac output and less severely elevated pulmonary vascular resistance.

2 change despite a significant decrease in the pulmonary vascular resistance.

3 lmonary vasculature associated with elevated pulmonary vascular resistance.

4 e pulmonary vasculature cause an increase in pulmonary vascular resistance.

5 pulmonary vasculature, leading to increased pulmonary vascular resistance.

6 extensive vascular remodeling and increased pulmonary vascular resistance.

7 ditional means to reverse extremely elevated pulmonary vascular resistance.

8 y reduced by a relative increase in regional pulmonary vascular resistance.

9 cs, left and right ventricular pressures and pulmonary vascular resistance.

10 pain inhibition were associated with reduced pulmonary vascular resistance.

11 mainstem bronchus occlusion to increase left pulmonary vascular resistance.

12 tionally decreased right atrial pressure and pulmonary vascular resistance.

13 ve increased pulmonary arterial pressure and pulmonary vascular resistance.

14 egarding the effects of iNO on regulators of pulmonary vascular resistance.

15 in decreased effects on thromboxane B(2) and pulmonary vascular resistance.

16 orrelate with pulmonary artery pressures and pulmonary vascular resistance.

17 h a high transpulmonary pressure gradient or pulmonary vascular resistance.

18 tion in mean pulmonary arterial pressure and pulmonary vascular resistance.

19 of distal pulmonary arterioles and increased pulmonary vascular resistance.

20 ation and oxygenation, and does not increase pulmonary vascular resistance.

21 nce and oxygenation while avoiding increased pulmonary vascular resistance.

22 ents negatively correlated (rho=-0.497) with pulmonary vascular resistance.

23 re, right atrial pressure, cardiac index and pulmonary vascular resistance.

24 HT deaths occurred in patients with elevated pulmonary vascular resistance.

25 is a significant correlation between PED and pulmonary vascular resistance.

26 bacteremia-induced increases in systemic and pulmonary vascular resistances.

27 /- 35 vs. 245 +/- 39 m; P < 0.05); decreased pulmonary vascular resistance (0.18 +/- 0.02 vs. 0.38 +/

28 -41 dyne/s per cm(-5); P<0.001), and isoflow pulmonary vascular resistance (124+/-74 dyne/s per cm(-5

29 ssure (60.5 [13.8] vs 56.4 [15.3] mm Hg) and pulmonary vascular resistance (16.6 [8.3] vs 12.9 [8.3]

30 (21, 27, 27 cm2, respectively; P<0.005), and pulmonary vascular resistance (2.4, 2.9, 3.6 woods units

31 pressure (53.4 mm Hg versus 49.5 mm Hg) and pulmonary vascular resistance (2.6 WU versus 2.3 WU; P<0

32 3.0 versus 14.5+/-3.5 mm Hg; P=0.05), higher pulmonary vascular resistance (2.6+/-1.6 versus 2.0+/-1.

33 /- 9.7 vs. 12.16 +/- 11 mmHg, P = 0.005; and pulmonary vascular resistance, 226.5 +/- 135 vs. 140.7 +

34 87.8+/-18.3% predicted) and a higher resting pulmonary vascular resistance (247+/-101 versus 199+/-56

35 ry artery pressure (-8 mm Hg; p < 0.001) and pulmonary vascular resistance (-254 dyn x s x cm(-5); p

36 an pulmonary arterial pressure (-10%) and in pulmonary vascular resistance (-26%).

37 versus 36.6+/-5.7 versus 27.4+3.7 mm Hg) and pulmonary vascular resistance (294+/-158 versus 161+/-60

38 /- 7 versus 47 +/- 10 mm Hg, P < 0.0001) and pulmonary vascular resistance (3.0 +/- 1.4 versus 6.1 +/

39 2.5 g [IQR, 23.2-41.4]; P < 0.05) and median pulmonary vascular resistance (3.1 Wood units [IQR, 2.0-

40 Patients who died had higher pulmonary vascular resistance (3.8 +/- 1.6 Wood units [W

41 , wedge capillary pressure 18 (16-22) mm Hg, pulmonary vascular resistance 362 (235-603) dyn s cm(-5)

42 nge (0/7 versus 140/1055 [13.2%]), had lower pulmonary vascular resistance (5.2+/-3.1 versus 10.5+/-7

43 Among recipients with high pulmonary vascular resistance, 5-year survival was simil

44 RV afterload was similar in SScPAH and IPAH (pulmonary vascular resistance=7.0+/-4.5 versus 7.9+/-4.3

45 ncrease in heart rate, 236+/-54% increase in pulmonary vascular resistance, 71+/-27% increase in syst

46 5 versus mutation carriers 55+/-9 mm Hg) and pulmonary vascular resistance (755 [483-1043] versus 931

47 mean pulmonary artery pressure (49 mmHg) and pulmonary vascular resistance (8.5 Woods units) were con

48 1.8 mm Hg; p = 0.005) and tended to decrease pulmonary vascular resistance (-83 +/- 33 dynes; p = 0.0

49 ide (NO) plays an important part in lowering pulmonary vascular resistance after birth, and in persis

50 ty liquid lung ventilation resulted in lower pulmonary vascular resistance after bypass compared with

51 0.01); functional class, cardiac index, and pulmonary vascular resistance also improved (p < 0.02 fo

52 Cardiac index and pulmonary vascular resistance also improved on long-term

53 Prostacyclin (PGI(2)) reduces pulmonary vascular resistance and attenuates vascular sm

54 ruitment maneuvers (RM) may adversely affect pulmonary vascular resistance and cardiac filling or per

55 eriod when patients may experience increased pulmonary vascular resistance and decreased ventricular

56 idonic acid caused dose-related increases in pulmonary vascular resistance and decreases in systemic

57 We conclude that rhSOD reduces pulmonary vascular resistance and facilitates the action

58 pulmonary arterial hypertension, would lower pulmonary vascular resistance and improve exercise capac

59 perative period, would a) selectively reduce pulmonary vascular resistance and improve RV hemodynamic

60 Sildenafil reduced pulmonary vascular resistance and increased cardiac outp

61 n reduced mean pulmonary artery pressure and pulmonary vascular resistance and increased cardiac outp

62 ressure, mean pulmonary artery pressure, and pulmonary vascular resistance and increased cardiac outp

63 reduced mean pulmonary arterial pressure and pulmonary vascular resistance and increased transpulmona

64 ons, but to date, there are no data on basal pulmonary vascular resistance and its responsiveness to

65 e BACS and prostaglandin groups showed lower pulmonary vascular resistance and less arterial stiffnes

66 ong linear relationship also existed between pulmonary vascular resistance and minimum septal curvatu

67 dient, transpulmonary pressure gradient, and pulmonary vascular resistance and more pronounced ventil

68 SCD with RHC-confirmed PH who have elevated pulmonary vascular resistance and normal pulmonary capil

69 LRM and PEEP decreased pulmonary vascular resistance and normalized ventilation

70 ces between the treatment groups, except for pulmonary vascular resistance and oxygen extraction, per

71 the eNOS gene in vivo can selectively reduce pulmonary vascular resistance and pulmonary pressor resp

72 l pulmonary arteries, resulting in increased pulmonary vascular resistance and pulmonary pressures.

73 High pulmonary vascular resistance and right atrial pressure

74 by neointimal lesions, resulting in elevated pulmonary vascular resistance and right heart failure.

75 LA dysfunction was associated with increased pulmonary vascular resistance and right ventricular dysf

76 factorial disease characterized by increased pulmonary vascular resistance and right ventricular fail

77 y disease causes cor pulmonale with elevated pulmonary vascular resistance and secondary reductions i

78 Pulmonary vascular resistance and vascular permeability

79 al pulmonary arteries, resulting in elevated pulmonary vascular resistance and, eventually, in right

80 Adding surfactant before EVLP returned PaO2, pulmonary vascular resistance, and apoptotic-cell percen

81 time, LVAD, retransplantation, pretransplant pulmonary vascular resistance, and immunologic variables

82 a results in a detrimental increase in total pulmonary vascular resistance, and increased load on the

83 pressure, systemic vascular resistance, and pulmonary vascular resistance, and increased resting and

84 educed exercise pulmonary arterial pressure, pulmonary vascular resistance, and pulmonary vascular re

85 for diagnosis, WHO functional class, indexed pulmonary vascular resistance, and pulmonary-to-systemic

86 rvival when adjusted for pulmonary pressure, pulmonary vascular resistance, and right atrial pressure

87 of the distal pulmonary arteries, increased pulmonary vascular resistance, and right ventricular dys

88 extending the pediatric limits on acceptable pulmonary vascular resistance, and risk prediction of pe

89 ces, maintenance of appropriate systemic and pulmonary vascular resistance, and surgical planning and

90 ry capillary wedge pressure, cardiac output, pulmonary vascular resistance, and systemic vascular res

91 Hypocarbic alkalosis acutely reduced hypoxic pulmonary vascular resistance, and this was sustained fo

92 eased mean arterial pressure*, systemic* and pulmonary* vascular resistances, and atrial natriuretic

93 d changes in right ventricular (RV) mass and pulmonary vascular resistance as co-primary endpoints an

94 l improved the primary end point of exercise pulmonary vascular resistance as compared with placebo (

95 at a .Q of less than 10 L.min(-1) or a total pulmonary vascular resistance at exercise of less than 3

96 As compared to pulmonary vascular resistance at rest, slope of increase

97 ke volume responses to exertion, but similar pulmonary vascular resistance at rest.

98 The primary endpoint was pulmonary vascular resistance at week 12, expressed as r

99 es in gas exchange, hemodynamic function, or pulmonary vascular resistance between the two groups.

100 Changes in cardiac index, systemic and pulmonary vascular resistance, blood pressure, and heart

101 Intravenous beta-agonists reduce pulmonary vascular resistance but are not suitable for c

102 ressure was attributed to an increase in the pulmonary vascular resistance, but for all nine patients

103 ulmonary arterial pressure by 13 +/- 2%, and pulmonary vascular resistance by 36 +/- 8% (all p < 0.05

104 naling in the hypoxic mouse lung and reduced pulmonary vascular resistance by attenuating vascular re

105 84+/-23.6 mL; P=0.003), with marked falls in pulmonary vascular resistance (by 29%; P=0.03) and right

106 There was some discrepancy between pulmonary vascular resistance calculated by flow derived

107 ic data including pulmonary artery pressure, pulmonary vascular resistance, capillary wedge pressure,

108 nce index, presence of pericardial effusion, pulmonary vascular resistance, cardiac index, and right

109 adjustment for potential mediators including pulmonary vascular resistance, cardiac index, and vasore

110 - 20 months, resulting in a 71% reduction in pulmonary vascular resistance compared to baseline.

111 ith FI(O(2)) = 1.00, rhSOD treatment lowered pulmonary vascular resistance compared with control anim

112 raction (+7.6% +/- 1.5%; p = 0.032), whereas pulmonary vascular resistance decreased (-202 +/- 65 dyn

113 Mean pulmonary artery pressure and pulmonary vascular resistance decreased (64 +/- 3 mm Hg

114 The pulmonary vascular resistance decreased along with the r

115 Pulmonary vascular resistance decreased by 223 dyn s cm(

116 Pulmonary vascular resistance decreased by 226 dyn.sec.c

117 Pulmonary vascular resistance decreased by 379 dyne.s.cm

118 reased 26%; cardiac output increased by 22%; pulmonary vascular resistance decreased by 42%; and the

119 The pulmonary vascular resistance decreased from 1143 dynes

120 Pulmonary vascular resistance decreased with exercise in

121 lary PH with elevated vascular gradients and pulmonary vascular resistance defines combined post- and

122 e compared with preoperative partitioning of pulmonary vascular resistance derived from the occlusion

123 remained unchanged in nonsurvivors, whereas pulmonary vascular resistance did not change in either g

124 The cardiac index and pulmonary vascular resistance did not change significant

125 The primary end point was pulmonary vascular resistance during exercise.

126 Pulmonary vascular resistance (dynes.sec.cm) increased f

127 itor group (23 min, CI: 21-25) (P<0.05), and pulmonary vascular resistance elevation and complement a

128 at is characterized by a progressive rise in pulmonary vascular resistance, eventually leading to rig

129 NO significantly improved pulmonary vascular resistance (excluding the initial col

130 4 to 4 +/- 0.74 liter/min/M2 (p = 0.01), and pulmonary vascular resistance from 3.7 +/- 1.7 to 4.7 +/

131 ater can also occur in the setting of normal pulmonary vascular resistance from a high flow state and

132 mPAP of 35 mm Hg or greater, with increased pulmonary vascular resistance from portopulmonary hypert

133 a mean pulmonary artery pressure > 25 mm Hg, pulmonary vascular resistance > 240 dynes x second x cm(

134 k trial, evaluated imatinib in patients with pulmonary vascular resistance >/= 800 dyne.s.cm(-5) symp

135 lmonary artery wedge pressure >15 mm Hg; (2) pulmonary vascular resistance >/=3.0 Wood units; or (3)

136 pulmonary artery pressure of >/=38 mm Hg and pulmonary vascular resistance >/=425 dynes.s(-1).cm(-5)

137 y diastolic mitral annular velocity >14, and pulmonary vascular resistance >2.5 Wood units, accuratel

138 ad mean pulmonary artery pressure >25 mm Hg, pulmonary vascular resistance >240 dyn-sec/cm(-5) , and

139 >/=35 mm Hg) and 28 (34%) also had increased pulmonary vascular resistance >3.0 WU.

140 associated with increased mortality included pulmonary vascular resistance >32 Wood units (hazard rat

141 PAH, 6-minute walk distance </=450 m, and a pulmonary vascular resistance >800 dynes.s/cm(5), despit

142 survival was lower for recipients with high pulmonary vascular resistance (>4 Woods units; P=0.02).

143 mean pulmonary artery pressure, >/=25 mm Hg; pulmonary vascular resistance, >3.0 WU; pulmonary artery

144 Elevated pulmonary vascular resistance has been associated with r

145 confidence interval, 1.03-1.13; P<0.01), and pulmonary vascular resistance (hazard ratio, 1.01; 95% c

146 compliance; 95% CI, 1.02-1.37; p = 0.03) and pulmonary vascular resistance (hazard ratio, 1.28 per in

147 -2.79 per 10 mm Hg increase; P = 0.011), and pulmonary vascular resistance (HR, 1.44; 95% CI, 1.09-1.

148 lting in increased mean airway pressures and pulmonary vascular resistance in both sham and intestina

149 d mean pulmonary artery pressure and indexed pulmonary vascular resistance in children with pulmonary

150 monary vascular remodeling and the increased pulmonary vascular resistance in hypoxic pulmonary hyper

151 effective capillary pressure, we partitioned pulmonary vascular resistance in larger arterial (upstre

152 as to create a model for estimating mPAP and pulmonary vascular resistance in patients with chronic t

153 significantly improved exercise capacity and pulmonary vascular resistance in patients with chronic t

154 rrelation between flow-mediated dilation and pulmonary vascular resistance in patients with HFpEF and

155 liferation is a major cause for the elevated pulmonary vascular resistance in patients with idiopathi

156 Because of high pulmonary vascular resistance in patients with primary p

157 e reduction of pulmonary artery pressure and pulmonary vascular resistance in piglets with hypoxia-in

158 Macitentan significantly improved pulmonary vascular resistance in portopulmonary hyperten

159 We hypothesized that increased pulmonary vascular resistance in PPH would reduce the ra

160 t on gas exchange, lung compliance (CL), and pulmonary vascular resistance in premature animals with

161 a type 5 phosphodiesterase inhibitor, lowers pulmonary vascular resistance in pulmonary hypertension

162 xygen delivery and a significant increase in pulmonary vascular resistance in the post-bypass period.

163 0.4 +/- 0.1 L/min/m2 (n = 27, p = 0.01), and pulmonary vascular resistance increased 3 +/- 1 Wood uni

164 rom 44+/-9% to 24+/-17% (P:=0.0220), and the pulmonary vascular resistance increased from 2.0+/-0.9 t

165 PTT, LV FWHM, and LV TTP correlated with pulmonary vascular resistance index (P < .01), right ven

166 in mean pulmonary artery pressure (MPAP) and pulmonary vascular resistance index (PVRI) (by 9.6% and

167 ated with mean PAP (r = 0.62, P < .0014) and pulmonary vascular resistance index (PVRI) (r = 0.77, P

168 ase, but the potential relationships between pulmonary vascular resistance index (PVRI) and Fontan fa

169 mary study endpoint was a fall from baseline pulmonary vascular resistance index (PVRi) of 20% or mor

170 stolic pulmonary artery pressure (sPAP), and pulmonary vascular resistance index (PVRI).

171 The median pulmonary vascular resistance index (Rpi) was 6.0 WU/m(2

172 nd antiprostacyclin antibody group, elevated pulmonary vascular resistance index and pulmonary artery

173 om 1513 to 1225 dyne x sec/cm5 x m2, and the pulmonary vascular resistance index decreased from 723 t

174 Pulmonary vascular resistance index was also an independ

175 iagnosis, mean pulmonary artery pressure and pulmonary vascular resistance index were 56 mm Hg and 17

176 When controlling for pulmonary vascular resistance index, graft ischemic time

177 ight ventricular systolic pressure and total pulmonary vascular resistance index, increased pulmonary

178 sed survival from enrollment included higher pulmonary vascular resistance index, lower-weight z scor

179 o groups based on whether their preoperative pulmonary vascular resistance indicated severe or nonsev

180 HPV, as reflected by the increase in left pulmonary vascular resistance induced by left mainstem b

181 Pulmonary vascular resistance is an important hemodynami

182 Preoperative pulmonary vascular resistance is an independent risk fac

183 Pulmonary vascular resistance is frequently elevated in

184 Pulmonary vascular resistance is frequently increased in

185 rial compliance remains predictive even when pulmonary vascular resistance is normal.

186 e characterized by a progressive increase in pulmonary vascular resistance leading to right heart fai

187 disease defined by a progressive increase in pulmonary vascular resistance leading to right-sided hea

188 (HPV), we measured the increase in left lung pulmonary vascular resistance (LPVR) before and during h

189 uring endotoxemia, the increase in left lung pulmonary vascular resistance (LPVR) before and during l

190 nt (mean PAP minus mean PAWP) <12 mm Hg, and pulmonary vascular resistance </=3 Wood units (WU).

191 Furthermore, in the setting of high pulmonary vascular resistance, male recipients who recei

192 ecreased pulmonary artery systolic pressure, pulmonary vascular resistance, mean pulmonary artery pre

193 Subsequently, pulmonary vascular resistance, microvascular permeabilit

194 echnique that has been used for partitioning pulmonary vascular resistance, might identify CTEPH pati

195 Arterial oxygenation (PaO(2), mm Hg), pulmonary vascular resistance (mm Hg/mL per minute), rec

196 end points included changes from baseline in pulmonary vascular resistance, N-terminal pro-brain natr

197 Secondary end points included the change in pulmonary vascular resistance, N-terminal pro-brain natr

198 epoprostenol, defined by a reduction in the pulmonary vascular resistance of > or =25%, was achieved

199 rresponding to a ratio of geometric mean for pulmonary vascular resistance of 0.65 (95% CI 0.59-0.72,

200 onary artery pressure of 45 (10) mm Hg and a pulmonary vascular resistance of 10.7 (4.2) Wood units.

201 nute walk distance of 50 m or more, and with pulmonary vascular resistance of 320 dyn.s.cm(-5) or mor

202 lary wedge pressure of 22.6+/-8.9 mm Hg, and pulmonary vascular resistance of 4.6+/-2.9 Wood units.

203 r resistance was overestimated by calculated pulmonary vascular resistance on the basis of PC-MRI in

204 nary embolism caused a four-fold increase in pulmonary vascular resistance (p < 0.0001) and a two-fol

205 an pulmonary arterial pressure (p < 0.0001), pulmonary vascular resistance (p = 0.008), right ventric

206 h lower right atrial pressure (P = 0.02) and pulmonary vascular resistance (P = 0.01) in men with PAH

207 servoir strain was associated with increased pulmonary vascular resistance (P<0.0001) and decreased p

208 There were significant improvements in pulmonary vascular resistance (P<0.001), NT-proBNP level

209 th mean pulmonary arterial pressure and left pulmonary vascular resistance (P:<0.05).

210 easures of pulmonary arterial compliance and pulmonary vascular resistance predict mortality in acute

211 Exercise intolerance is multifactorial, but pulmonary vascular resistance probably plays a crucial r

212 cular septal defect and a marked increase in pulmonary vascular resistance (pulmonary obstructive dis

213 d pulmonary hypertension in mice, decreasing pulmonary vascular resistance, pulmonary artery remodeli

214 mean pulmonary artery pressure >=25 mm Hg or pulmonary vascular resistance (PVR) > 400 dyn s cm(-5) b

215 Patients with pulmonary vascular resistance (PVR) >4 WU or right ventr

216 In group 1, O2 decreased pulmonary vascular resistance (PVR) (mean+/-SEM) from 17

217 Additionally, pulmonary vascular resistance (PVR) 2.2 to 3.0 WU, consi

218 nce 28 +/- 3 versus 29 +/- 2 (Cstat-cm H2O), pulmonary vascular resistance (PVR) 593 +/- 127 versus 4

219 ry hypertension and the relationship between pulmonary vascular resistance (PVR) and exercise cardiac

220 to play an important role in maintaining low pulmonary vascular resistance (PVR) and in modulating pu

221 onary hypertension associated with increased pulmonary vascular resistance (PVR) and occurring in the

222 ionship was shown between 48 h postoperative pulmonary vascular resistance (PVR) and walking and stai

223 S II) contributes to the NO-mediated fall in pulmonary vascular resistance (PVR) at birth, we studied

224 An elevated pulmonary vascular resistance (PVR) before LT was associ

225 ulmonary hypertension, INO decreased PAP and pulmonary vascular resistance (PVR) but did not affect M

226 elium-derived nitric oxide (NO) and lowering pulmonary vascular resistance (PVR) by passive recruitme

227 erentiating patients with primarily elevated pulmonary vascular resistance (PVR) from those with PH p

228 er pulmonary pulse pressure), in relation to pulmonary vascular resistance (PVR) in heart failure.

229 Accurate determination of pulmonary vascular resistance (PVR) is an important comp

230 R) to monitor acute and long-term changes in pulmonary vascular resistance (PVR) noninvasively.

231 in mean pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) of 16.4 and 32.7%, r

232 ntified as WHO functional class II-IV with a pulmonary vascular resistance (PVR) of at least 400 dyn.

233 The increase in pulmonary vascular resistance (PVR) seen in children aft

234 al exercise, the transpulmonary gradient and pulmonary vascular resistance (PVR) were elevated in the

235 to mean pulmonary artery pressure (mPAP) and pulmonary vascular resistance (PVR) with additional rece

236 The primary end point was change in pulmonary vascular resistance (PVR) with exercise.

237 in mean pulmonary arterial pressure (mPAP), pulmonary vascular resistance (PVR), and cardiac index.

238 d pulmonary artery systolic pressure (PASP), pulmonary vascular resistance (PVR), and pulmonary arter

239 d in a significant rise in mean PA pressure, pulmonary vascular resistance (PVR), and RV stroke work

240 gram/kg/min) significantly decreased Ppa and pulmonary vascular resistance (PVR), but these pulmonary

241 ignificantly reduces pulmonary pressures and pulmonary vascular resistance (PVR), effects reverse rig

242 Both groups showed a rapid rise in pulmonary vascular resistance (PVR), which is a characte

243 ontan procedure depends in large part on low pulmonary vascular resistance (PVR).

244 essure (PAOP), and resistance via calculated pulmonary vascular resistance (PVR).

245 es a clinically reliable method to determine pulmonary vascular resistance (PVR).

246 othelin-1 (ET), and ET levels correlate with pulmonary vascular resistance (PVR).

247 tan mean pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR).

248 0% in mean pulmonary artery (PA) pressure or pulmonary vascular resistance (PVR).

249 ion (PH) in children involves measurement of pulmonary vascular resistance (PVR); however, PVR neglec

250 an pulmonary arterial pressure >25 mm Hg and pulmonary vascular resistance [PVR] >/=240 dynes.s.cm) w

251 ing right atrial pressure, mean PA pressure, pulmonary vascular resistance [PVR], and PVR and PA pres

252 t stroke volume (r = 0.660; p < 0.0001), and pulmonary vascular resistance (r = 0.643; p = 0.001) cor

253 heses that, unlike the systemic circulation, pulmonary vascular resistance (R(PA)) and compliance (C(

254 rongly with degree of PH (r=0.66; P<0.0001), pulmonary vascular resistance (r=0.60; P<0.0001), and ri

255 nspulmonary gradient (r=0.560; P=0.013), and pulmonary vascular resistance (r=0.626; P=0.004).

256 O2 correlated directly with baseline resting pulmonary vascular resistance (r=0.74, P=0.002) and indi

257 ght ventricular-pulmonary arterial coupling (pulmonary vascular resistance: R=-0.36; P<0.01; right ve

258 ed RAP/PCWP ratio was associated with higher pulmonary vascular resistance, reduced RV function (mani

259 change in mean pulmonary artery pressure and pulmonary vascular resistance, respectively (r=0.58 and

260 rterial remodeling that results in increased pulmonary vascular resistance, right ventricular (RV) fa

261 pulmonary arteries, leading to elevation of pulmonary vascular resistance, right ventricular failure

262 artery pressure (PPA) and incremental total pulmonary vascular resistance (RPI) were greater in NOS3

263 Furthermore, PYR reduced pulmonary vascular resistance, RV afterload, and pulmona

264 Calpain inhibition prevented the increased pulmonary vascular resistance seen in control animals (9

265 ly nor late death was influenced by elevated pulmonary vascular resistance, sensitization, prior LVAD

266 A medication capable of decreasing pulmonary vascular resistance should allow improved card

267 sion pressure, systemic vascular resistance, pulmonary vascular resistance, shunt fraction, and alveo

268 placed had significantly higher preoperative pulmonary vascular resistance, significantly higher comm

269 pressure, pulmonary vascular resistance, and pulmonary vascular resistance/systemic vascular resistan

270 of nitric oxide is vital for the decrease in pulmonary vascular resistance that normally occurs after

271 od palliation often requires manipulation of pulmonary vascular resistance to alter the pulmonary-to-

272 ally restore pulmonary arterial pressure and pulmonary vascular resistance to near levels measured in

273 eek 12, the geometric mean ratio of baseline pulmonary vascular resistance was 0.63 (95% CI 0.58-0.67

274 Their indexed pulmonary vascular resistance was 1.8 (1.2-2.3) W/m(2),

275 ork Heart Association class >/=III, and mean pulmonary vascular resistance was 11.2+/-6.4 WU.

276 ry artery pressure was 60+/-2 mm Hg, average pulmonary vascular resistance was 1664+/-81 dyne x s x c

277 rdiac index was 3.5 +/- 0.9 L/min/m(2) , and pulmonary vascular resistance was 5.6 +/- 2.8 Wood units

278 The attenuation in pulmonary vascular resistance was associated with a blun

279 previously found that the postnatal fall in pulmonary vascular resistance was associated with actin

280 Alkalosis caused sustained vasodilation when pulmonary vascular resistance was high but either failed

281 liance remained predictive of mortality when pulmonary vascular resistance was in the normal range (p

282 In nonsuitable group, pulmonary vascular resistance was increased at FiO2 of 0

283 dCMVeNOS) on pulmonary arterial pressure and pulmonary vascular resistance was investigated in eNOS-d

284 Pulmonary vascular resistance was normal (<1.5 Wood Unit

285 Pulmonary vascular resistance was overestimated by calcu

286 group (26.4+/-1.5, 42.4+/-6.6 ms, P=0.003); pulmonary vascular resistance was significantly lower in

287 ated pulmonary artery wedge pressure and low pulmonary vascular resistance, we make a strong recommen

288 -9.0 to -3.0 mm Hg), and the mean changes in pulmonary vascular resistance were -4.6 and 0.9 mm Hg/L

289 Mean pulmonary artery pressure and pulmonary vascular resistance were acquired at baseline

290 iastolic relaxation time constant (tau), and pulmonary vascular resistance were determined.

291 Elevated PAP and pulmonary vascular resistance were not risk factors.

292 eductions in pulmonary arterial pressure and pulmonary vascular resistance were noted.

293 tion in mean pulmonary arterial pressure and pulmonary vascular resistance when compared with values

294 ctivity, histological lung injury score, and pulmonary vascular resistance while systemic arterial pr

295 Furthermore, male recipients with elevated pulmonary vascular resistance who received hearts from f

296 However, recipients with elevated pulmonary vascular resistance who received undersized he

297 se of the augmented effect of iNO decreasing pulmonary vascular resistance with high-frequency oscill

298 epresented a 35% (95% CI 28-41) reduction in pulmonary vascular resistance with macitentan versus pla

299 le effect on pulmonary arterial pressure and pulmonary vascular resistance, without systemic hypotens

300 15, p = 0.323; Q = 3.82, I(2) = 21.42%), and pulmonary vascular resistance (WMD: -1.42 dyn*s/cm(5), 9