ライフサイエンスコーパス: vascular resistance

1 st amongst patients with the lowest systemic vascular resistance.

2 hese augmentations were driven by changes in vascular resistance.

3 atrial pressure, cardiac index and pulmonary vascular resistance.

4 estimated from characteristic impedance and vascular resistance.

5 nced sodium retention and increased systemic vascular resistance.

6 occurred in patients with elevated pulmonary vascular resistance.

7 ficant correlation between PED and pulmonary vascular resistance.

8 cal pressure, and variations in the systemic vascular resistance.

9 creating transient hypoxemia and increasing vascular resistance.

10 ned by cardiac output (total flow) and total vascular resistance.

11 r smooth muscle cell activation and elevated vascular resistance.

12 duced in placentas associated with increased vascular resistance.

13 ved cardiac index and pulmonary and systemic vascular resistance.

14 output and less severely elevated pulmonary vascular resistance.

15 pite a significant decrease in the pulmonary vascular resistance.

16 ed resistance for venous return and systemic vascular resistance.

17 lood flow, suggesting a reduction in hepatic vascular resistance.

18 tal (cold) stress, and higher basal systemic vascular resistance.

19 nd right ventricular pressures and pulmonary vascular resistance.

20 esults initially from increased intrahepatic vascular resistance.

21 ranspulmonary pressure gradient or pulmonary vascular resistance.

22 dulation of cardiac output and/or peripheral vascular resistance.

23 pulmonary arterioles and increased pulmonary vascular resistance.

24 lts in elevated blood pressure and increased vascular resistance.

25 ue, in part, through reduction of peripheral vascular resistance.

26 oxygenation, and does not increase pulmonary vascular resistance.

27 tion, and lowers blood pressure and systemic vascular resistance.

28 tion are not deleterious in terms of in vivo vascular resistance.

29 ygenation while avoiding increased pulmonary vascular resistance.

30 rterial flow, indicating increased placental vascular resistance.

31 ively correlated (rho=-0.497) with pulmonary vascular resistance.

32 245 +/- 39 m; P < 0.05); decreased pulmonary vascular resistance (0.18 +/- 0.02 vs. 0.38 +/- 0.14 mm

33 hypertension decreased 8[13, 4] mmHg, as did vascular resistance 1.5[2.2, 0.9] WU, and transmural rig

34 re (28 +/- 5 mm Hg; p < 0.0001) and systemic vascular resistance (1,320 +/- 143 dynes; p < 0.0001) co

35 72 +/- 0.2 mm Hg/mL; p < 0.001) and systemic vascular resistance (+1,812 +/- 767 dynes; p < 0.001) wi

36 per cm(-5); P<0.001), and isoflow pulmonary vascular resistance (124+/-74 dyne/s per cm(-5) versus 9

37 Patients with CSPH had lower systemic vascular resistance (1336 +/- 423 versus 1469 +/- 335 dy

38 93 +/- 2 mm Hg, flow 310 +/- 20 mL/min, and vascular resistance 153 +/- 16 mm Hg/L per minute.

39 5 [13.8] vs 56.4 [15.3] mm Hg) and pulmonary vascular resistance (16.6 [8.3] vs 12.9 [8.3] Wood units

40 ltration rate (21%, p<0.05), decreased renal vascular resistance (18%, p<0.05) but caused no signific

41 7 cm2, respectively; P<0.005), and pulmonary vascular resistance (2.4, 2.9, 3.6 woods units, respecti

42 (53.4 mm Hg versus 49.5 mm Hg) and pulmonary vascular resistance (2.6 WU versus 2.3 WU; P<0.001 for b

43 14.5+/-3.5 mm Hg; P=0.05), higher pulmonary vascular resistance (2.6+/-1.6 versus 2.0+/-1.0 Wood uni

44 rkload with improved cardiac index and lower vascular resistance, 2) upgraded hearts' apelinergic res

45 interval of indirect effect including renal vascular resistance, -2.51 to -0.76).

46 12.16 +/- 11 mmHg, P = 0.005; and pulmonary vascular resistance, 226.5 +/- 135 vs. 140.7 +/- 123.7 d

47 nterval, -89.4 to -3.8; P=0.03) and systemic vascular resistance (-239.3 dynes.s(-1).cm(-5); 95% conf

48 ptic shock associated with elevated systemic vascular resistance (2C); and use of hydrocortisone only

49 s 47 +/- 10 mm Hg, P < 0.0001) and pulmonary vascular resistance (3.0 +/- 1.4 versus 6.1 +/- 3.1 Wood

50 , 23.2-41.4]; P < 0.05) and median pulmonary vascular resistance (3.1 Wood units [IQR, 2.0-5.7] vs. 6

51 Patients who died had higher pulmonary vascular resistance (3.8 +/- 1.6 Wood units [WU] vs. 2.1

52 pillary pressure 18 (16-22) mm Hg, pulmonary vascular resistance 362 (235-603) dyn s cm(-5).

53 NO3(-) led to greater reductions in systemic vascular resistance (-42.4+/-16.6% versus -31.8+/-20.3%;

54 ersus 140/1055 [13.2%]), had lower pulmonary vascular resistance (5.2+/-3.1 versus 10.5+/-7.0 Wood un

55 ad was similar in SScPAH and IPAH (pulmonary vascular resistance=7.0+/-4.5 versus 7.9+/-4.3 Wood unit

56 utation carriers 55+/-9 mm Hg) and pulmonary vascular resistance (755 [483-1043] versus 931 [624-1311

57 nary artery pressure (49 mmHg) and pulmonary vascular resistance (8.5 Woods units) were consistent wi

58 p = 0.005) and tended to decrease pulmonary vascular resistance (-83 +/- 33 dynes; p = 0.07).

59 s 6.6 +/- 0.4 L/min, p < 0.05), but systemic vascular resistance (885 +/- 77 dyn.s/cm vs 531 +/- 29 d

60 e renal plasma flow and an increase in renal vascular resistance (all P<0.01).

61 eption of cardiac index and indexed systemic vascular resistance, all the other hepatic and systemic

62 be dynamic to avoid the increase in systemic vascular resistance and abrupt changes in intrathoracic

63 Kir2 channels also regulate vascular resistance and blood pressure.

64 endothelial glycocalyx) results in increased vascular resistance and disturbed endothelial nitric oxi

65 ranscription and secretion, raising systemic vascular resistance and early heritable responses to env

66 Furthermore, negative correlations between vascular resistance and hematocrit are observed in vario

67 The regenerated endothelium showed reduced vascular resistance and improved barrier function over t

68 ean pulmonary artery pressure, and pulmonary vascular resistance and increased cardiac output and ind

69 mean pulmonary artery pressure and pulmonary vascular resistance and increased cardiac output.

70 condary to significant decreases in systemic vascular resistance and increases in stroke volume compa

71 Increased vascular resistance and left ventricular mass were the m

72 prostaglandin groups showed lower pulmonary vascular resistance and less arterial stiffness.

73 nsatory mechanism for the blunted peripheral vascular resistance and lower central volume.

74 relationship also existed between pulmonary vascular resistance and minimum septal curvature indexed

75 nspulmonary pressure gradient, and pulmonary vascular resistance and more pronounced ventilatory resp

76 RHC-confirmed PH who have elevated pulmonary vascular resistance and normal pulmonary capillary wedge

77 LRM and PEEP decreased pulmonary vascular resistance and normalized ventilation/perfusion

78 y arteries, resulting in increased pulmonary vascular resistance and pulmonary pressures.

79 Increased vascular resistance and reduced fetoplacental blood flow

80 nts mean systemic filling pressure, systemic vascular resistance and resistance for venous return inc

81 High pulmonary vascular resistance and right atrial pressure by invasiv

82 mal lesions, resulting in elevated pulmonary vascular resistance and right heart failure.

83 tion was associated with increased pulmonary vascular resistance and right ventricular dysfunction in

84 disease characterized by increased pulmonary vascular resistance and right ventricular failure; morbi

85 ion during HMP resulted in lower endischemic vascular resistance and slightly elevated free radical-m

86 In contrast, the decline in peripheral vascular resistance and the increase in nitric oxide are

87 Because RBC aggregation promotes vascular resistance and thrombosis, W could also provide

88 Pulmonary vascular resistance and vascular permeability measured i

89 or CPASMCs in controlling both fetoplacental vascular resistance and vasculogenesis.

90 ry arteries, resulting in elevated pulmonary vascular resistance and, eventually, in right ventricula

91 tly reduced systemic arterial compliance and vascular resistances and increased valvulo-arterial impe

92 lower arterial afterload (decreased systemic vascular resistance) and higher metabolic rate.

93 factors (cardiac output, blood pressure and vascular resistance) and how these change with sex and a

94 ulature of target organs that operate at low vascular resistance, and abnormal ventricular-arterial i

95 factant before EVLP returned PaO2, pulmonary vascular resistance, and apoptotic-cell percentage to sh

96 leads to endothelial dysfunction, increased vascular resistance, and arterial remodeling and stiffen

97 luding renal artery pulsatility index, renal vascular resistance, and arterial volume in the cortex,

98 levated cardiac stroke volume with decreased vascular resistance, and elevated pressor responses to e

99 arget genes, liver injury, increased hepatic vascular resistance, and endothelial dysfunction.

100 proved uterine blood flow, decreased uterine vascular resistance, and improved fetal weights in compa

101 evaluated by mean pulmonary artery pressure, vascular resistance, and limited vascular remodeling qua

102 Cardiac output, systemic vascular resistance, and mean arterial blood pressure we

103 sis, WHO functional class, indexed pulmonary vascular resistance, and pulmonary-to-systemic arterial

104 n adjusted for pulmonary pressure, pulmonary vascular resistance, and right atrial pressure and provi

105 stal pulmonary arteries, increased pulmonary vascular resistance, and right ventricular dysfunction t

106 the pediatric limits on acceptable pulmonary vascular resistance, and risk prediction of pediatric tr

107 es, as well as indices of vascular function (vascular resistance, aortic input impedance, compliance,

108 in right ventricular (RV) mass and pulmonary vascular resistance as co-primary endpoints and stroke v

109 the primary end point of exercise pulmonary vascular resistance as compared with placebo (-0.6+/-0.5

110 e arterial elastance was related to systemic vascular resistance at baseline (r = 0.89) and fluid-ind

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

112 As compared to pulmonary vascular resistance at rest, slope of increase in pulmon

113 responses to exertion, but similar pulmonary vascular resistance at rest.

114 The primary endpoint was pulmonary vascular resistance at week 12, expressed as ratio of ba

115 opolysaccharide binding protein and systemic vascular resistance below the mean (1,011 dynes x s/cm(5

116 put (beta=0.20, P<0.0001) and lower systemic vascular resistance (beta=-0.18, P<0.0001).

117 put (beta=-0.10, P<0.05) and higher systemic vascular resistance (beta=0.08, P<0.05), whereas lower b

118 Intravenous beta-agonists reduce pulmonary vascular resistance but are not suitable for chronic use

119 Higher third trimester umbilical artery vascular resistance, but not uterine artery vascular res

120 Higher third trimester feto-placental vascular resistance, but not utero-placental vascular re

121 the hypoxic mouse lung and reduced pulmonary vascular resistance by attenuating vascular remodeling.

122 mL; P=0.003), with marked falls in pulmonary vascular resistance (by 29%; P=0.03) and right atrial pr

123 cluding pulmonary artery pressure, pulmonary vascular resistance, capillary wedge pressure, and cardi

124 presence of pericardial effusion, pulmonary vascular resistance, cardiac index, and right atrial pre

125 for potential mediators including pulmonary vascular resistance, cardiac index, and vasoreactivity.

126 e drives mechanisms that increase peripheral vascular resistance causing hypertension.

127 athetic activity may fail to produce greater vascular resistance changes in hypertensive rats because

128 Coronary vascular resistance (CVR; mean arterial pressure/coronar

129 Persistent increased vascular resistance damages vascular endothelial cells-a

130 7.6% +/- 1.5%; p = 0.032), whereas pulmonary vascular resistance decreased (-202 +/- 65 dynes; p = 0.

131 The pulmonary vascular resistance decreased along with the ratio of th

132 Pulmonary vascular resistance decreased by 226 dyn.sec.cm(-5) in t

133 Pulmonary vascular resistance decreased by 379 dyne.s.cm(-5) (95%

134 Pulmonary vascular resistance decreased with exercise in all contr

135 a late increase in heart rate, whereas total vascular resistance decreased.

136 th elevated vascular gradients and pulmonary vascular resistance defines combined post- and precapill

137 Carotid artery pressure, blood flow and vascular resistance did not change compared to fetuses r

138 unchanged in nonsurvivors, whereas pulmonary vascular resistance did not change in either group.

139 al elastance (femoral estimate) and systemic vascular resistance did not change.

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

141 arguing a vital role for S1P in maintaining vascular resistance during recovery from circulatory sho

142 ed effective arterial elastance and systemic vascular resistance (each p < 0.05).

143 on the OCS system due to prohibitively high vascular resistance, edema, and worsening compliance.

144 e face of increased cardiac output, systemic vascular resistance fails to decline homeostatically.

145 BP in salt resistance, renal and peripheral vascular resistance falls and is associated with an incr

146 g led to an acute increase in uterine artery vascular resistance, fetal peripheral vasoconstriction,

147 lso occur in the setting of normal pulmonary vascular resistance from a high flow state and/or increa

148 5 mm Hg or greater, with increased pulmonary vascular resistance from portopulmonary hypertension, ha

149 es in heart rate, blood pressure and forearm vascular resistance (FVR) during submaximal LBNP.

150 valuated imatinib in patients with pulmonary vascular resistance >/= 800 dyne.s.cm(-5) symptomatic on

151 tery wedge pressure >15 mm Hg; (2) pulmonary vascular resistance >/=3.0 Wood units; or (3) inpatient

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

153 c mitral annular velocity >14, and pulmonary vascular resistance >2.5 Wood units, accurately identifi

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

155 g) and 28 (34%) also had increased pulmonary vascular resistance >3.0 WU.

156 nute walk distance </=450 m, and a pulmonary vascular resistance >800 dynes.s/cm(5), despite therapy

157 nary artery pressure, >/=25 mm Hg; pulmonary vascular resistance, >3.0 WU; pulmonary artery wedge pre

158 Elevated pulmonary vascular resistance has been associated with raised leve

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

160 ; 95% CI, 1.02-1.37; p = 0.03) and pulmonary vascular resistance (hazard ratio, 1.28 per interquartil

161 10 mm Hg increase; P = 0.011), and pulmonary vascular resistance (HR, 1.44; 95% CI, 1.09-1.89 per Woo

162 rect effect of INT-747 on total intrahepatic vascular resistance (IHVR) and intrahepatic vascular ton

163 sms that regulate the increased intrahepatic vascular resistance (IHVR) in cirrhosis.

164 In cirrhosis, increased intrahepatic vascular resistance (IHVR) is the primary factor for por

165 breathing (SDB) is associated with increased vascular resistance in children and adults.

166 monary artery pressure and indexed pulmonary vascular resistance in children with pulmonary hypertens

167 cular remodeling and the increased pulmonary vascular resistance in hypoxic pulmonary hypertension.

168 capillary pressure, we partitioned pulmonary vascular resistance in larger arterial (upstream resista

169 te a model for estimating mPAP and pulmonary vascular resistance in patients with chronic thromboembo

170 tly improved exercise capacity and pulmonary vascular resistance in patients with chronic thromboembo

171 between flow-mediated dilation and pulmonary vascular resistance in patients with HFpEF and PH (r=-0.

172 Macitentan significantly improved pulmonary vascular resistance in portopulmonary hypertension patie

173 Resistance for venous return and systemic vascular resistance increased more (p = 0.019 and p = 0.

174 essure (-7 mm Hg; p = 0.041) and in systemic vascular resistance index (-116 dyne.sec/cm5/m2; p = 0.0

175 t (28 vs 11 cm H(2)O; P < .001) and systemic vascular resistance index (1610 vs 1384 dyn . sec . cm(-

176 , and heart rate (7%) and decreased systemic vascular resistance index (21%), whereas mean arterial p

177 - 0.79 mm Hg.m(2)/mL; P<0.0001) and systemic vascular resistance index (3116 +/- 799 versus 2515 +/-

178 V FWHM, and LV TTP correlated with pulmonary vascular resistance index (P < .01), right ventricular s

179 ide (p = 0.001; 95% CI, 0.99-1.00), systemic vascular resistance index (p < 0.001; 95% CI, 0.97-0.99)

180 ducing mean arterial pressure and peripheral vascular resistance index (P<0.001 for all) irrespective

181 lmonary artery pressure (MPAP) and pulmonary vascular resistance index (PVRI) (by 9.6% and 20.8%, res

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

183 he potential relationships between pulmonary vascular resistance index (PVRI) and Fontan failure have

184 endpoint was a fall from baseline pulmonary vascular resistance index (PVRi) of 20% or more over 16

185 =0.02) in the sildenafil group, and systemic vascular resistance index (resting, P=0.0002; peak exerc

186 n children and to analyze the correlation of vascular resistance index (RI) and the degree of vascula

187 oppler callus vascularity was visualized and vascular resistance index (RI) was measured.

188 al compliance (pulsatile load), and systemic vascular resistance index (steady load) were compared be

189 The systemic vascular resistance index (SVRI) was estimated from the

190 The aim was to investigate systemic vascular resistance index (SVRI), cardiac index, and myo

191 ressure), arterial load properties (systemic vascular resistance index and elastance index) and chang

192 eptic sheep, MAP fell by ~30 mm Hg, systemic vascular resistance index decreased by ~50%, and ~7 L of

193 index (P=0.005) increased, whereas systemic vascular resistance index decreased during exercise (P<0

194 Systemic vascular resistance index was not associated with diasto

195 Systemic vascular resistance index was reduced (P<0.0001-interact

196 pliance was lower in women, whereas systemic vascular resistance index was similar between sexes.

197 changes in stroke volume index and systemic vascular resistance index were measured within the first

198 total arterial compliance, Ca; and systemic vascular resistance index) in patients with LGSAS (mean

199 nal pro-B-type natriuretic peptide, systemic vascular resistance index, and stroke volume index on da

200 When controlling for pulmonary vascular resistance index, graft ischemic time, and card

201 icular systolic pressure and total pulmonary vascular resistance index, increased pulmonary artery ac

202 ased on whether their preoperative pulmonary vascular resistance indicated severe or nonsevere chroni

203 iance remains predictive even when pulmonary vascular resistance is normal.

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

205 cardiac output with no changes in peripheral vascular resistance may contribute to (pre)syncope.

206 -12%; P<0.001) and pulmonary (-29%; P=0.002) vascular resistance, mean pulmonary artery (-25%; P<0.00

207 monstrated a significant correlation between vascular resistance measured in vivo and ex vivo in norm

208 y may significantly influence the intrarenal vascular resistance measured using Doppler sonography in

209 clearance (index of GFR) and increased renal vascular resistance (measured by transit time nanoprobes

210 included changes from baseline in pulmonary vascular resistance, N-terminal pro-brain natriuretic pe

211 end points included the change in pulmonary vascular resistance, N-terminal pro-brain natriuretic pe

212 g to a ratio of geometric mean for pulmonary vascular resistance of 0.65 (95% CI 0.59-0.72, p<0.0001)

213 ry pressure of 45 (10) mm Hg and a pulmonary vascular resistance of 10.7 (4.2) Wood units.

214 distance of 50 m or more, and with pulmonary vascular resistance of 320 dyn.s.cm(-5) or more without

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

216 ability of astronauts to augment peripheral vascular resistance, often resulting in orthostatic hypo

217 ic sinus eddy vortices and variable systemic vascular resistance on overall valve opening-closing dyn

218 ce was overestimated by calculated pulmonary vascular resistance on the basis of PC-MRI in comparison

219 d by other mechanisms that increase coronary vascular resistance or reduce coronary driving pressure.

220 ed physiological variables (lung compliance, vascular resistance, oxygenation capacity), lung weight

221 ism caused a four-fold increase in pulmonary vascular resistance (p < 0.0001) and a two-fold increase

222 o hypoxia resulted in a decrease of systemic vascular resistance (p < 0.0001) and diastolic blood pre

223 ry arterial pressure (p < 0.0001), pulmonary vascular resistance (p = 0.008), right ventricular arter

224 ght atrial pressure (P = 0.02) and pulmonary vascular resistance (P = 0.01) in men with PAH.

225 rain was associated with increased pulmonary vascular resistance (P<0.0001) and decreased peak oxygen

226 e were significant improvements in pulmonary vascular resistance (P<0.001), NT-proBNP levels (P<0.001

227 pulmonary arterial compliance and pulmonary vascular resistance predict mortality in acute respirato

228 intolerance is multifactorial, but pulmonary vascular resistance probably plays a crucial role.

229 activity is an efficient mechanism to raise vascular resistance promptly, corroborating its involvem

230 y hypertension in mice, decreasing pulmonary vascular resistance, pulmonary artery remodeling, and ri

231 nary artery pressure >=25 mm Hg or pulmonary vascular resistance (PVR) > 400 dyn s cm(-5) based on ri

232 Patients with pulmonary vascular resistance (PVR) >4 WU or right ventricular dys

233 Additionally, pulmonary vascular resistance (PVR) 2.2 to 3.0 WU, considered prev

234 3 versus 29 +/- 2 (Cstat-cm H2O), pulmonary vascular resistance (PVR) 593 +/- 127 versus 495 +/- 70

235 An elevated pulmonary vascular resistance (PVR) before LT was associated with

236 g patients with primarily elevated pulmonary vascular resistance (PVR) from those with PH predominant

237 ry pulse pressure), in relation to pulmonary vascular resistance (PVR) in heart failure.

238 tor acute and long-term changes in pulmonary vascular resistance (PVR) noninvasively.

239 WHO functional class II-IV with a pulmonary vascular resistance (PVR) of at least 400 dyn.s/cm(5) an

240 lmonary artery pressure (mPAP) and pulmonary vascular resistance (PVR) with additional receiver opera

241 ulmonary arterial pressure (mPAP), pulmonary vascular resistance (PVR), and cardiac index.

242 y artery systolic pressure (PASP), pulmonary vascular resistance (PVR), and pulmonary arterial compli

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

244 ry arterial pressure >25 mm Hg and pulmonary vascular resistance [PVR] >/=240 dynes.s.cm) who were ap

245 atrial pressure, mean PA pressure, pulmonary vascular resistance [PVR], and PVR and PA pressure-flow

246 olume (r = 0.660; p < 0.0001), and pulmonary vascular resistance (r = 0.643; p = 0.001) correlated si

247 h degree of PH (r=0.66; P<0.0001), pulmonary vascular resistance (r=0.60; P<0.0001), and right ventri

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

249 cular-pulmonary arterial coupling (pulmonary vascular resistance: R=-0.36; P<0.01; right ventricular

250 , which were coupled with increased cerebral vascular resistance, reduced cerebral blood flow, and a

251 decreased cardiac index, increased systemic vascular resistance, reduced portal pressure (PP), super

252 P ratio was associated with higher pulmonary vascular resistance, reduced RV function (manifest as a

253 as effective arterial elastance and systemic vascular resistance remained unchanged.

254 mean pulmonary artery pressure and pulmonary vascular resistance, respectively (r=0.58 and -0.74; P<0

255 rterial volume in the cortex or higher renal vascular resistance, respectively, when offered as media

256 ion, and function through reduction in renal vascular resistance, reversal of endothelial dysfunction

257 modeling that results in increased pulmonary vascular resistance, right ventricular (RV) failure, and

258 Furthermore, PYR reduced pulmonary vascular resistance, RV afterload, and pulmonary vascula

259 rats may be due to a reduction in peripheral vascular resistance since epicardial lidocaine significa

260 sly recorded and cardiac output and systemic vascular resistance (SVR) assessed at 30-minute interval

261 ), cardiac contractility (iCON) and systemic vascular resistances (sVR) were simultaneously monitored

262 athetic activity produces greater changes in vascular resistance than tonic stimulation of the same s

263 significantly to the increased intrahepatic vascular resistance that is the primary cause of portal

264 culatory support and an increase in systemic vascular resistance that leads to reduced vasopressor us

265 g mechanisms regulating sodium excretion and vascular resistance, they generate similar haemodynamic

266 system adjusts cardiac output and peripheral vascular resistance to changing physiological demands.

267 We conclude that MetS confers vascular resistance to GLP-1 receptor agonists, partiall

268 e is required to maintain local and systemic vascular resistance under physiological and pathological

269 her heart rate, and lower blood pressure and vascular resistance values.

270 nin-angiotensin system and directly controls vascular resistance, vessel contractility, and remodelin

271 g patterns, revealed that bursting increases vascular resistance (VR) more than tonic stimulation (57

272 e geometric mean ratio of baseline pulmonary vascular resistance was 0.63 (95% CI 0.58-0.67) in the m

273 Their indexed pulmonary vascular resistance was 1.8 (1.2-2.3) W/m(2), and mean p

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

275 x was 3.5 +/- 0.9 L/min/m(2) , and pulmonary vascular resistance was 5.6 +/- 2.8 Wood units.

276 Finally, elevated cerebral vascular resistance was a predictor of hypertension, sug

277 Causally, cerebral vascular resistance was elevated before the onset of hyp

278 ained predictive of mortality when pulmonary vascular resistance was in the normal range (p = 0.02).

279 In nonsuitable group, pulmonary vascular resistance was increased at FiO2 of 0.21 compar

280 Pulmonary vascular resistance was overestimated by calculated pulm

281 of peripheral organs was increased, systemic vascular resistance was reduced and cardiac output and l

282 In perfused FGR placentas, vascular resistance was significantly elevated compared

283 vascular resistance, but not uterine artery vascular resistance, was associated with higher childhoo

284 vascular resistance, but not utero-placental vascular resistance, was associated with slower fetal gr

285 nary artery wedge pressure and low pulmonary vascular resistance, we make a strong recommendation aga

286 Mean pulmonary artery pressure and pulmonary vascular resistance were acquired at baseline and during

287 third trimester umbilical and uterine artery vascular resistance were associated with lower fetal len

288 in effective arterial elastance and systemic vascular resistance were correlated (r = 0.88).

289 ssure gradient, cardiac output, and systemic vascular resistance were made at baseline and after 4 we

290 ients with HFrEF leads to increased systemic vascular resistance, which constrains stroke volume, car

291 eedback in HFrEF leads to increased systemic vascular resistance, which constrains stroke volume, car

292 is mediated by a selective reduction in BAT vascular resistance, which greatly increases vascular pe

293 One of the hallmarks is a rise of peripheral vascular resistance, which largely depends on arteriole

294 increased retention of sodium and water and vascular resistance, which lead to the further developme

295 lso induced tachycardia and loss of systemic vascular resistance, which were not seen with local appl

296 istological lung injury score, and pulmonary vascular resistance while systemic arterial pressure was

297 d right heart filling pressures and systemic vascular resistance, while increasing cardiac and stroke

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

299 Because most of the vascular resistance within the brain is in capillaries,

300 323; Q = 3.82, I(2) = 21.42%), and pulmonary vascular resistance (WMD: -1.42 dyn*s/cm(5), 95%CI: -72.