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

1 lmonary vasculature associated with elevated pulmonary vascular resistance.

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

3 pulmonary vasculature, leading to increased pulmonary vascular resistance.

4 extensive vascular remodeling and increased pulmonary vascular resistance.

5 ditional means to reverse extremely elevated pulmonary vascular resistance.

6 nce and oxygenation while avoiding increased pulmonary vascular resistance.

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

8 pain inhibition were associated with reduced pulmonary vascular resistance.

9 mainstem bronchus occlusion to increase left pulmonary vascular resistance.

10 tionally decreased right atrial pressure and pulmonary vascular resistance.

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

12 ve increased pulmonary arterial pressure and pulmonary vascular resistance.

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

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

15 orrelate with pulmonary artery pressures and pulmonary vascular resistance.

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

17 ease in mean pulmonary arterial pressure and pulmonary vascular resistance.

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

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

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

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

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

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

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

25 /- 35 vs. 245 +/- 39 m; P < 0.05); decreased pulmonary vascular resistance (0.18 +/- 0.02 vs. 0.38 +/

26 -41 dyne/s per cm(-5); P<0.001), and isoflow pulmonary vascular resistance (124+/-74 dyne/s per cm(-5

27 al volume was increased from 10 to 20 mL/kg, pulmonary vascular resistance (1351 +/- 94 vs. 2266 +/-

28 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]

29 pressure (2 +/- 9% vs. 0 +/- 6%, p = NS) and pulmonary vascular resistance (19 +/- 25% vs. 11 +/- 32%

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

31 3.0 versus 14.5+/-3.5 mm Hg; P=0.05), higher pulmonary vascular resistance (2.6+/-1.6 versus 2.0+/-1.

32 87.8+/-18.3% predicted) and a higher resting pulmonary vascular resistance (247+/-101 versus 199+/-56

33 decreased systemic vascular resistance 24%, pulmonary vascular resistance 25%, pulmonary capillary w

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

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

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

37 /- 7 versus 47 +/- 10 mm Hg, P < 0.0001) and pulmonary vascular resistance (3.0 +/- 1.4 versus 6.1 +/

38 2.5 g [IQR, 23.2-41.4]; P < 0.05) and median pulmonary vascular resistance (3.1 Wood units [IQR, 2.0-

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

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

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

42 [SEM] to 4.7 +/- 0.4 mL/cm) and increases in pulmonary vascular resistance (68 +/- 6.4 vs. 91.9 +/- 8

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

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

45 5 versus mutation carriers 55+/-9 mm Hg) and pulmonary vascular resistance (755 [483-1043] versus 931

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

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

48 0.01); functional class, cardiac index, and pulmonary vascular resistance also improved (p < 0.02 fo

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

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

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

52 Pulmonary vascular resistance and characteristic impedan

53 s on the cardiovascular system by increasing pulmonary vascular resistance and characteristic impedan

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

55 ases in mean pulmonary arterial pressure and pulmonary vascular resistance and decreases in mean arte

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

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

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

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

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

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

71 High pulmonary vascular resistance and right atrial pressure

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

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

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

75 Pulmonary vascular resistance and vascular permeability

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 crease pulmonary vascular cGMP levels, lower pulmonary vascular resistance, augment iNO-induced pulmo

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

94 , long-term therapy with epoprostenol lowers pulmonary vascular resistance beyond the level achieved

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

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

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

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

99 84+/-23.6 mL; P=0.003), with marked falls in pulmonary vascular resistance (by 29%; P=0.03) and right

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

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

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

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

104 - 20 months, resulting in a 71% reduction in pulmonary vascular resistance compared to baseline.

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

106 ptoms and hemodynamic measures, and overall, pulmonary vascular resistance declined by 53 percent to

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

108 The pulmonary vascular resistance decreased along with the r

109 Pulmonary vascular resistance decreased by 223 dyn s cm(

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

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

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

113 The pulmonary vascular resistance decreased from 1143 dynes

114 Both pulmonary arterial mean pressure and pulmonary vascular resistance decreased significantly wi

115 Pulmonary vascular resistance decreased with exercise in

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

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

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

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

120 At rest, systemic and pulmonary vascular resistance (dyne . s-1 . cm-5) increa

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

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

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

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

125 Compared with room air, pulmonary vascular resistance fell 36% with NO (P<0.001)

126 4 to 4 +/- 0.74 liter/min/M2 (p = 0.01), and pulmonary vascular resistance from 3.7 +/- 1.7 to 4.7 +/

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

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

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

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

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

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

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

134 >/=35 mm Hg) and 28 (34%) also had increased pulmonary vascular resistance >3.0 WU.

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

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

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

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

139 Elevated pulmonary vascular resistance has been associated with r

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

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

142 -2.79 per 10 mm Hg increase; P = 0.011), and pulmonary vascular resistance (HR, 1.44; 95% CI, 1.09-1.

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

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

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

146 NO) therapy improves gas exchange and lowers pulmonary vascular resistance in neonates and children w

147 NONOate would improve oxygenation and reduce pulmonary vascular resistance in oleic acid-induced acut

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

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

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

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

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

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

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

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

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

157 Decrease in pulmonary vascular resistance in response to acute vasod

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

159 0.4 +/- 0.1 L/min/m2 (n = 27, p = 0.01), and pulmonary vascular resistance increased 3 +/- 1 Wood uni

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

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

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

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

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

165 AEP/NO animals had significant reductions in pulmonary vascular resistance index (PVRI) and MPAP at a

166 ethyl ester (1 to 2 mg/kg IV) had raised the pulmonary vascular resistance index (PVRI) from 4.4+/-0.

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

168 he DMAEP/NO group had a greater reduction in pulmonary vascular resistance index (PVRI) than did cont

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

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

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

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

173 pic transplantation was performed unless the pulmonary vascular resistance index remained >6 um2 (des

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 iagnosis, cardiac hemodynamics (particularly pulmonary vascular resistance index), donor ischemic tim

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

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

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

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

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

182 Pulmonary vascular resistance is an important hemodynami

183 Preoperative pulmonary vascular resistance is an independent risk fac

184 Pulmonary vascular resistance is frequently elevated in

185 Pulmonary vascular resistance is frequently increased in

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

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

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

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

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

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

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

193 travenous adenosine had a variable effect on pulmonary vascular resistance (mean reduction, 27 percen

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

195 Subsequently, pulmonary vascular resistance, microvascular permeabilit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

216 ) is a crucial mediator in the regulation of pulmonary vascular resistance (PVR) and VSM proliferatio

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

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

219 vascular tone and contributes to the fall in pulmonary vascular resistance (PVR) at birth.

220 ts of NO on the longitudinal distribution of pulmonary vascular resistance (PVR) before and after end

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

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

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

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

225 Nitric oxide (NO) modulates pulmonary vascular resistance (PVR) in the normal fetus

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

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

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

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

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

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

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

233 n in mean pulmonary artery pressure (mPA) or pulmonary vascular resistance (PVR) with the vasodilator

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

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

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

237 Pulmonary vascular resistance (PVR), lung dynamic compli

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

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

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

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

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

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

244 0% in mean pulmonary artery (PA) pressure or pulmonary vascular resistance (PVR).

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

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

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

248 pulmonary artery pressure (Ppa) and indexed pulmonary vascular resistance (PVRI) without affecting m

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

280 Pulmonary vascular resistance was normal (<1.5 Wood Unit

281 Pulmonary vascular resistance was overestimated by calcu

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

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

284 -9.0 to -3.0 mm Hg), and the mean changes in pulmonary vascular resistance were -4.6 and 0.9 mm Hg/L

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

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

287 Their mean pulmonary arterial pressure and pulmonary vascular resistance were greater as well (not

288 Left pulmonary artery flow and pulmonary vascular resistance were measured at 30-min in

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

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

291 significant increases in the PA pressure and pulmonary vascular resistance were observed in MCTP dogs

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

293 progressive disease characterised by raised pulmonary vascular resistance, which results in diminish

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 A significant decrease in pulmonary vascular resistance with an oral nifedipine ch

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

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