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

1 n LV end-diastolic pressure, heart rate, and systemic vascular resistance.

2 ce (end-systolic pressure/stroke volume) and systemic vascular resistance.

3 lmonary vascular resistance and decreases in systemic vascular resistance.

4 te vasodilation, which critically influences systemic vascular resistance.

5 re the information and the monitoring of the systemic vascular resistance.

6 ved: 1) parasympathetic, 2) inotropy, and 3) systemic vascular resistance.

7 d a slight increase in arterial pressure and systemic vascular resistance.

8 capillary wedge pressure, cardiac index, or systemic vascular resistance.

9 ar relaxation, and lowers blood pressure and systemic vascular resistance.

10 ere poorest amongst patients with the lowest systemic vascular resistance.

11 ere inversely correlated with the changes in systemic vascular resistance.

12 lume, pulmonary capillary wedge pressure and systemic vascular resistance.

13 g to enhanced sodium retention and increased systemic vascular resistance.

14 y, underlying etiologies, volume status, and systemic vascular resistance.

15 .03] P=0.048), with no significant effect on systemic vascular resistance.

16 ractility and, to a lesser extent, to reduce systemic vascular resistance.

17 , but contribute little to reflex control of systemic vascular resistance.

18 vortex local pressure, and variations in the systemic vascular resistance.

19 and improved cardiac index and pulmonary and systemic vascular resistance.

20 calculated resistance for venous return and systemic vascular resistance.

21 nvironmental (cold) stress, and higher basal systemic vascular resistance.

22 thermia paralleled by an initial increase in systemic vascular resistance.

23 n dp/dtmax, end-systolic blood pressure, and systemic vascular resistance.

24 g aorta (constant flow) provided an index of systemic vascular resistance.

25 ge or mean arterial pressure, heart rate, or systemic vascular resistance.

26 ncreased nitric oxide synthesis, and reduced systemic vascular resistance.

27 d with the absence of significant changes in systemic vascular resistance.

28 ful guide to left ventricular afterload than systemic vascular resistance.

29 left ventricular end-diastolic pressure and systemic vascular resistance.

30 low constant) were used to assess changes in systemic vascular resistance.

31 c indices and reduced arterial pressures and systemic vascular resistances.

32 indices and reduced arterial pressures, and systemic vascular resistances.

33 od pressure (28 +/- 5 mm Hg; p < 0.0001) and systemic vascular resistance (1,320 +/- 143 dynes; p < 0

34 ance (+0.72 +/- 0.2 mm Hg/mL; p < 0.001) and systemic vascular resistance (+1,812 +/- 767 dynes; p <

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

36 +/- 3.4 mm Hg at baseline, 3, and 5 hrs) and systemic vascular resistance (1498 +/- 53, 788 +/- 37, 8

37 wedge pressure (32+/-3 to 15+/-2 mm Hg), and systemic vascular resistance (1581+/-200 to 938+/-63 dyn

38 o 15+/-5 mm Hg early; 12+/-6 mm Hg late) and systemic vascular resistance (1651+/-369 to 1207+/-281 d

39 8% vs. 40 +/- 18%, p = NS) and a decrease in systemic vascular resistance (22 +/- 13% vs. 24 +/- 11%,

40 fidence interval, -89.4 to -3.8; P=0.03) and systemic vascular resistance (-239.3 dynes.s(-1).cm(-5);

41 Vessel dilator decreased systemic vascular resistance 24%, pulmonary vascular res

42 However, there was also a fall in the systemic vascular resistance (-26.2+/-12.8%, P<0.005) an

43 output septic shock associated with elevated systemic vascular resistance (2C); and use of hydrocorti

44 /min; cardiac index, 6.4 +/- 0.4 L/min/min2; systemic vascular resistance, 326 +/- 107 dyne cm/s2).

45 /- 24.4 to 188.3 +/- 30.8 ml/min per m2) and systemic vascular resistance (36.8 +/- 8 to 21.9 +/- 5.5

46 17 +/- 2 versus 11 +/- 2 mm Hg; P < .05) and systemic vascular resistance (3891 +/- 379 versus 3071 +

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

48 ressure (57+/-4 to 84+/-2 mm Hg, P<.001) and systemic vascular resistance (813+/-113 to 1188+/-87 dyn

49 4 L/min vs 6.6 +/- 0.4 L/min, p < 0.05), but systemic vascular resistance (885 +/- 77 dyn.s/cm vs 531

50 terial pressure (69+/-8 to 93+/-4 mm Hg) and systemic vascular resistance (898+/-88 to 1443+/-72 dyne

51 ure have decreased cardiac output, increased systemic vascular resistance, abnormal diastolic functio

52 e index, diastolic blood pressure, and total systemic vascular resistance all were significantly lowe

53 atic venous pressures, as well as the lowest systemic vascular resistance (all p <0.01).

54 h the exception of cardiac index and indexed systemic vascular resistance, all the other hepatic and

55 ease by 6 h), mean right atrial pressure and systemic vascular resistance, along with significant inc

56 The animals' heart rates and systemic vascular resistances also did not change.

57 =19) had an initial considerable increase in systemic vascular resistance and a decrease in cardiac o

58 s attributable to either a large increase in systemic vascular resistance and a decrease in cardiac o

59 is associated with a significant increase in systemic vascular resistance and a relatively minor incr

60 e has to be dynamic to avoid the increase in systemic vascular resistance and abrupt changes in intra

61 itions, including afterload as determined by systemic vascular resistance and arterial elastance (Ea)

62 th a strict requirement for its HBD, reduces systemic vascular resistance and arterial pressure in a

63 The use of AT(1)RB decreased systemic vascular resistance and attenuated local expres

64 Low systemic vascular resistance and bradycardia are also co

65 The systemic vascular resistance and cardiac contractility w

66 The systemic vascular resistance and dynamic response charac

67 nce NPY transcription and secretion, raising systemic vascular resistance and early heritable respons

68 including endothelial dysfunction, increased systemic vascular resistance and elevated systemic and p

69 trial, systolic and mean arterial pressures, systemic vascular resistance and haematocrit were not di

70 s characterized by hypotension and decreased systemic vascular resistance and impaired vascular react

71 Short-term intravenous bosentan reduced systemic vascular resistance and improved overall LV per

72 with congestive heart failure by decreasing systemic vascular resistance and improving ventricular d

73 ed arterial and central venous pressures and systemic vascular resistance and increased heart rate, c

74 Significantly decreased systemic vascular resistance and increased left ventricu

75 HFrEF secondary to significant decreases in systemic vascular resistance and increases in stroke vol

76 cular responders) or b) smaller increases in systemic vascular resistance and no change or an increas

77 ascular responders) or a smaller increase in systemic vascular resistance and no change or an increas

78 ble individuals are unable to increase their systemic vascular resistance and plasma noradrenaline co

79 n of SQBNP, cardiac output was increased and systemic vascular resistance and pulmonary capillary wed

80 e peak effect of dipyridamole on heart rate, systemic vascular resistance and pulmonary capillary wed

81 Systemic vascular resistance and pulmonary vascular resi

82 ysaccharide resulted in greater increases in systemic vascular resistance and pupillary mydriasis and

83 all patients mean systemic filling pressure, systemic vascular resistance and resistance for venous r

84 nificantly higher mean arterial pressure and systemic vascular resistance and significantly lower por

85 the use of afterload reduction to stabilize systemic vascular resistance and therefore the pulmonary

86 emic reduction of Hb concentration decreased systemic vascular resistance and TO2 and increased heart

87 to both lower arterial afterload (decreased systemic vascular resistance) and higher metabolic rate.

88 ificant changes in PaO2, oxygen consumption, systemic vascular resistance, and cardiac output through

89 exhibits a reduced systolic blood pressure, systemic vascular resistance, and cardiac stroke volume.

90 greater or earlier central venous pressures, systemic vascular resistance, and changes in the BUN:Cr

91 lling pressures of the left and right heart, systemic vascular resistance, and echocardiographic left

92 rome characterized by hypotension, decreased systemic vascular resistance, and elevated cardiac index

93 irculatory state with hypotension, decreased systemic vascular resistance, and increased cardiac outp

94 ated with substantial body growth, decreased systemic vascular resistance, and increased cardiac outp

95 oxygen delivery, increases in heart rate and systemic vascular resistance, and lactic acidosis.

96 Cardiac output, systemic vascular resistance, and mean arterial blood pr

97 reduced resting pulmonary arterial pressure, systemic vascular resistance, and pulmonary vascular res

98 ry vascular resistance, 71+/-27% increase in systemic vascular resistance, and up to a 100-fold incre

99 In the Fontan circulation, pulmonary and systemic vascular resistances are in series.

100 eded, decreased cardiac output and increased systemic vascular resistance as the most common hemodyna

101 cardiac output and stroke volume and reduce systemic vascular resistance as well as pulmonary capill

102 Therefore, the increase in systemic vascular resistance associated with ligation of

103 iovascular state (high cardiac index and low systemic vascular resistance) associated with endotoxin

104 Effective arterial elastance was related to systemic vascular resistance at baseline (r = 0.89) and

105 eased lipopolysaccharide binding protein and systemic vascular resistance below the mean (1,011 dynes

106 rdiac output (beta=0.20, P<0.0001) and lower systemic vascular resistance (beta=-0.18, P<0.0001).

107 rdiac output (beta=-0.10, P<0.05) and higher systemic vascular resistance (beta=0.08, P<0.05), wherea

108 An increase in systemic vascular resistance between two time points did

109 ere no differences in changes in heart rate, systemic vascular resistance, blood pressure, or renal f

110 njugate increased mean arterial pressure and systemic vascular resistance but did not influence cardi

111 Treatment with AT(1)RB decreased systemic vascular resistance but did not significantly i

112 significant increases in blood pressure and systemic vascular resistance but no changes in wall stre

113 put, oxygen content, oxygen consumption, and systemic vascular resistance, but were associated with s

114 in-13 reduced mean arterial pressure by ~4%, systemic vascular resistance by ~12%, and increased card

115 creased cardiac index (by 18%) and decreased systemic vascular resistance (by 11%), serum cholesterol

116 hemodynamic parameters like cardiac output, systemic vascular resistance, cardiac contractility, and

117 heart rate, stroke volume, cardiac output or systemic vascular resistance (conductance) responses to

118 Systemic vascular resistance declined with 30 mg (-564 d

119 ), cardiac output increased 9% (P=0.04), and systemic vascular resistance decreased 18% (P<0.001).

120 fluorescent microspheres) increased 46%, and systemic vascular resistance decreased by 21% (P < .001)

121 Systemic vascular resistance decreased from 1413+/-453 t

122 nary capillary wedge pressure decreased 44%, systemic vascular resistance decreased significantly, an

123 nary capillary wedge pressure decreased 52%, systemic vascular resistance decreased significantly, an

124 ve arterial elastance (femoral estimate) and systemic vascular resistance did not change.

125 ction fraction and cardiac output, and lower systemic vascular resistance during mental stress than p

126 d decreased effective arterial elastance and systemic vascular resistance (each p < 0.05).

127 ce, pulmonary artery pressure, pulmonary and systemic vascular resistances, ECG, serum cardiac enzyme

128 In the face of increased cardiac output, systemic vascular resistance fails to decline homeostati

129 During exercise, systemic vascular resistance fell in controls and AF but

130 During exercise, systemic vascular resistance fell, and there was no rela

131 During normoxia, L-NMMA increased systemic vascular resistance from 1,108 +/- 74 to 1,705

132 Acute hypoxia alone decreased systemic vascular resistance from 1,209 +/- 78 to 992 +/

133 +/- 18 ml (p < 0.001); and 3) a decrease in systemic vascular resistance from 1,226 +/- 481 dyn.s/cm

134 om 25 +/- 2 to 29 +/- 3 mm Hg, p < 0.05) and systemic vascular resistance (from 1,628 +/- 154 to 2,20

135 diac- and stroke volume index, pulmonary and systemic vascular resistance, heart rate, and blood pres

136 ary wedge pressure, and reduce pulmonary and systemic vascular resistance in initial clinical studies

137 e in the regulation of arterial pressure and systemic vascular resistance in this model of congestive

138 cant decreases in mean arterial pressure and systemic vascular resistance in TIVCC.

139 With CHF, systemic vascular resistance increased by 120%, was norm

140 P < .05) due to peripheral vasoconstriction (systemic vascular resistance increased from 644 to 1187

141 Resistance for venous return and systemic vascular resistance increased more (p = 0.019 a

142 blood pressure and pulse pressure, decreased systemic vascular resistance, increased aortic distensib

143 In the absence of a compensatory decrease in systemic vascular resistance, increases in plasma volume

144 terial pressure (-7 mm Hg; p = 0.041) and in systemic vascular resistance index (-116 dyne.sec/cm5/m2

145 (0.43 +/- 0.17 microg/kg/min; p = 0.002) and systemic vascular resistance index (1.44 +/- 0.57 dynes/

146 e gradient (28 vs 11 cm H(2)O; P < .001) and systemic vascular resistance index (1610 vs 1384 dyn . s

147 dex (15%), and heart rate (7%) and decreased systemic vascular resistance index (21%), whereas mean a

148 d 3.06 +/- 0.79 mm Hg.m(2)/mL; P<0.0001) and systemic vascular resistance index (3116 +/- 799 versus

149 hrs that was characterized by low values of systemic vascular resistance index (p < .05) and mean ar

150 ular response characterized by a decrease in systemic vascular resistance index (p < .05), and an inc

151 etic peptide (p = 0.001; 95% CI, 0.99-1.00), systemic vascular resistance index (p < 0.001; 95% CI, 0

152 ume index (range 10.5 to 29 mL/m2), and high systemic vascular resistance index (range 1,653 to 2,997

153 ercise (P=0.02) in the sildenafil group, and systemic vascular resistance index (resting, P=0.0002; p

154 al arterial compliance (pulsatile load), and systemic vascular resistance index (steady load) were co

155 The systemic vascular resistance index (SVRI) was estimated

156 red by effective arterial elastance (Ea) and systemic vascular resistance index (SVRI), and loading s

157 re were no differences between the groups in systemic vascular resistance index (SVRI), cardiac index

158 The aim was to investigate systemic vascular resistance index (SVRI), cardiac index

159 on of N omega-nitro-L-arginine methyl ester, systemic vascular resistance index and cardiac index ret

160 venous pressure), arterial load properties (systemic vascular resistance index and elastance index)

161 L-NMMA produced sustained increases in systemic vascular resistance index and mean arterial pre

162 , and oxygen delivery index and increases in systemic vascular resistance index and oxygen extraction

163 The co-primary endpoints were change in systemic vascular resistance index and renal blood flow.

164 s in pulmonary vascular resistance index and systemic vascular resistance index at 30 to 60 mins.

165 ure, pulmonary artery occlusion pressure, or systemic vascular resistance index between animals in gr

166 lmonary artery occlusive pressure, PVRI, and systemic vascular resistance index but also in the PaO(2

167 edly increased (p < .05, synergistic effect) systemic vascular resistance index compared with endotox

168 1.6 L/min at CPAP of 5 cm H2O, p < .05) and systemic vascular resistance index decreased (2412 +/- 5

169 In septic sheep, MAP fell by ~30 mm Hg, systemic vascular resistance index decreased by ~50%, an

170 esistance index (P=0.005) increased, whereas systemic vascular resistance index decreased during exer

171 ndex increased from 3.5 to 5.4 L/min/m2, the systemic vascular resistance index decreased from 1513 t

172 th SSPH and control animals (p < .05), while systemic vascular resistance index did not change.

173 .3 L/min at CPAP of 15 cm H2O, p < .005) and systemic vascular resistance index increased (2509 +/- 7

174 n rate at normothermia, leading to increased systemic vascular resistance index not seen at normother

175 Systemic vascular resistance index was not associated wi

176 Systemic vascular resistance index was reduced (P<0.0001

177 erial compliance was lower in women, whereas systemic vascular resistance index was similar between s

178 alysis of changes in stroke volume index and systemic vascular resistance index were measured within

179 ance, Ea; total arterial compliance, Ca; and systemic vascular resistance index) in patients with LGS

180 ance index, total arterial compliance index, systemic vascular resistance index), and clinical indice

181 dex, left ventricular stroke work index, and systemic vascular resistance index), metabolic parameter

182 dex, left ventricular stroke work index, and systemic vascular resistance index), metabolism (oxygen

183 cantly reduced mean arterial blood pressure, systemic vascular resistance index, and left ventricular

184 , MPAP, pulmonary artery occlusive pressure, systemic vascular resistance index, and PVRI, whereas ca

185 r N-terminal pro-B-type natriuretic peptide, systemic vascular resistance index, and stroke volume in

186 re, mean pulmonary arterial pressure (MPAP), systemic vascular resistance index, and urine output did

187 Heart rate, systemic vascular resistance index, left ventricular end

188 ficant differences between the two groups in systemic vascular resistance index, renal blood flow, me

189 n arterial pressure, MAP; cardiac index, CI; systemic vascular resistance index, SVRI; and stroke vol

190 ured mean arterial pressure, cardiac output, systemic vascular resistance index, the first derivative

191 HS 142-1 did not change systemic vascular resistance index.

192 ted with a potentiated (p < .05) increase in systemic vascular resistance index.

193 reased mean arterial pressure, pulmonary and systemic vascular resistance indices, and arterial and m

194 rmacologic reduction in filling pressure and systemic vascular resistance leads to a reduction in the

195 d decrease in cardiac output and increase in systemic vascular resistance noted in vascular responder

196 emptying but higher blood pressure (BP) and systemic vascular resistance occur in healthy older vers

197 ia during exercise, and greater increases in systemic vascular resistance occurred with ischemia duri

198 cing aortic sinus eddy vortices and variable systemic vascular resistance on overall valve opening-cl

199 eft ventricular preload and not by increased systemic vascular resistance or heart rate.

200 between maximum TNF-alpha concentrations and systemic vascular resistance (p < .01), cardiac index (p

201 xposure to hypoxia resulted in a decrease of systemic vascular resistance (p < 0.0001) and diastolic

202 stroke volume (p < 0.017) and an increase in systemic vascular resistance (p < 0.005).

203 c output, pulmonary vascular resistance, and systemic vascular resistance (P<0.05) compared with the

204 n stroke flow was related to the decrease in systemic vascular resistance (P=0.03), increase in total

205 essure, pulmonary artery occlusion pressure, systemic vascular resistance, pulmonary vascular resista

206 Systemic vascular resistance; PVL: 3.7 +/- 0.1 versus 4.

207 ary arterial pressure (PAP) and pulmonary to systemic vascular resistance ratio (PVR/SVR) were 34 +/-

208 esistance, and pulmonary vascular resistance/systemic vascular resistance ratio, which indicates a se

209 caffeine decreased cardiac index, increased systemic vascular resistance, reduced portal pressure (P

210 5), whereas effective arterial elastance and systemic vascular resistance remained unchanged.

211 al muscle blood flow, cardiac index (CI) and systemic vascular resistance responses to supine leg exe

212 tration for 10 weeks does not alter abnormal systemic vascular resistance, resting cardiac index, dia

213 Systemic vascular resistance returned toward baseline wi

214 cardiogenic shock severity, filling status, systemic vascular resistances rise, and adaptation to ch

215 The ratio of pulmonary and systemic vascular resistance (Rp:Rs) was determined at b

216 lso established weight-indexed pulmonary and systemic vascular resistances (Rpi and Rsi, respectively

217 the LPS groups, all agents elevated MAP and systemic vascular resistance similarly.

218 anges in the exercise-induced cardiac index, systemic vascular resistance, stroke volume, and VO(2) i

219 initial increase in cardiac output (CO) and systemic vascular resistance (SVR) as mixed responders w

220 continuously recorded and cardiac output and systemic vascular resistance (SVR) assessed at 30-minute

221 or cocaine evokes either a large increase in systemic vascular resistance (SVR) or a smaller increase

222 was designed to reduce filling pressures and systemic vascular resistance (SVR) without inotropic the

223 Vasodilation was defined by lower systemic vascular resistance (SVR), higher norepinephrin

224 lar resistance (PVR) but did not affect MAP, systemic vascular resistance (SVR), or CO.

225 c infusions have shown an opposite effect on systemic vascular resistance (SVR), possibly confounded

226 1), however, no differences were observed in systemic vascular resistance (SVR).

227 utput (CO), cardiac contractility (iCON) and systemic vascular resistances (sVR) were simultaneously

228 ecting mean aortic pressure (Pao) or indexed systemic vascular resistance (SVRI).

229 results in greater cardiac output and lower systemic vascular resistance than does single-chamber ve

230 vides circulatory support and an increase in systemic vascular resistance that leads to reduced vasop

231 systolic blood pressure, cardiac output, and systemic vascular resistance that were correlated with i

232 ere maintained, infusion of L-NMMA increased systemic vascular resistance (to 1,496 +/- 97 dynes-s-cm

233 ood pressure, stroke volume, cardiac output, systemic vascular resistance, total arterial compliance,

234 METHODS AND Systemic vascular resistance, total arterial compliance,

235 extraction above baseline, and decreases of systemic vascular resistance, total Hb, total solids, ar

236 e by augmenting cardiac indices, leaving the systemic vascular resistance unaffected.

237 genic tone is required to maintain local and systemic vascular resistance under physiological and pat

238 Systemic vascular resistance was inversely associated wi

239 ia the COX-2 pathway can alter pulmonary and systemic vascular resistance was investigated, and the e

240 iac index was significantly higher and total systemic vascular resistance was lower in all groups of

241 ere increased; b) plasma lactate was higher, systemic vascular resistance was lower, but ileal mucosa

242 erfusion of peripheral organs was increased, systemic vascular resistance was reduced and cardiac out

243 did not increase above baseline values, and systemic vascular resistance was unchanged following adm

244 /-0.6 and 3.7+/-0.4 L/min, and pulmonary and systemic vascular resistance were 312+/-134 and 2006+/-3

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

246 enous pressure gradient, cardiac output, and systemic vascular resistance were made at baseline and a

247 ate, pulmonary capillary wedge pressure, and systemic vascular resistance were measured throughout th

248 .01+/-0.26 L/min; P<0.001); the decreases in systemic vascular resistance were not different.

249 y correlated with mean arterial pressure and systemic vascular resistance, whereas levels of ADMA cor

250 ck in patients with HFrEF leads to increased systemic vascular resistance, which constrains stroke vo

251 fferent feedback in HFrEF leads to increased systemic vascular resistance, which constrains stroke vo

252 anaesthesia is caused by a rapid decrease in systemic vascular resistance, which makes alpha-agonists

253 tility, also induced tachycardia and loss of systemic vascular resistance, which were not seen with l

254 ate by increasing mean arterial pressure and systemic vascular resistance while decreasing cardiac in

255 h left and right heart filling pressures and systemic vascular resistance, while increasing cardiac a

256 -adrenergic mechanisms may serve to increase systemic vascular resistance with ageing, and that the e

257 dynamic response patterns: a) an increase in systemic vascular resistance with cardiac depression (va

258 temic vasodilatory reserve (ie, reduction in systemic vascular resistance with exercise) and quality

259 y capillary wedge pressure and pulmonary and systemic vascular resistances, with no change in heart r

260 hock) raised arterial pressure by increasing systemic vascular resistance without a significant prefe

261 ACE inhibitors decrease systemic vascular resistance without increasing heart ra