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1 ar relaxation, and lowers blood pressure and systemic vascular resistance.
2 lmonary vascular resistance and decreases in systemic vascular resistance.
3 te vasodilation, which critically influences systemic vascular resistance.
4 re the information and the monitoring of the systemic vascular resistance.
5 ved: 1) parasympathetic, 2) inotropy, and 3) systemic vascular resistance.
6 d a slight increase in arterial pressure and systemic vascular resistance.
7  capillary wedge pressure, cardiac index, or systemic vascular resistance.
8 vortex local pressure, and variations in the systemic vascular resistance.
9 ere inversely correlated with the changes in systemic vascular resistance.
10 lume, pulmonary capillary wedge pressure and systemic vascular resistance.
11 and improved cardiac index and pulmonary and systemic vascular resistance.
12 ere poorest amongst patients with the lowest systemic vascular resistance.
13  calculated resistance for venous return and systemic vascular resistance.
14 nvironmental (cold) stress, and higher basal systemic vascular resistance.
15 thermia paralleled by an initial increase in systemic vascular resistance.
16 n dp/dtmax, end-systolic blood pressure, and systemic vascular resistance.
17 g aorta (constant flow) provided an index of systemic vascular resistance.
18 ge or mean arterial pressure, heart rate, or systemic vascular resistance.
19 ncreased nitric oxide synthesis, and reduced systemic vascular resistance.
20 d with the absence of significant changes in systemic vascular resistance.
21 ful guide to left ventricular afterload than systemic vascular resistance.
22  left ventricular end-diastolic pressure and systemic vascular resistance.
23 g to enhanced sodium retention and increased systemic vascular resistance.
24 low constant) were used to assess changes in systemic vascular resistance.
25 n LV end-diastolic pressure, heart rate, and systemic vascular resistance.
26 ce (end-systolic pressure/stroke volume) and systemic vascular resistance.
27 c indices and reduced arterial pressures and systemic vascular resistances.
28  indices and reduced arterial pressures, and systemic vascular resistances.
29                 Patients with CSPH had lower systemic vascular resistance (1336 +/- 423 versus 1469 +
30 +/- 3.4 mm Hg at baseline, 3, and 5 hrs) and systemic vascular resistance (1498 +/- 53, 788 +/- 37, 8
31 wedge pressure (32+/-3 to 15+/-2 mm Hg), and systemic vascular resistance (1581+/-200 to 938+/-63 dyn
32 o 15+/-5 mm Hg early; 12+/-6 mm Hg late) and systemic vascular resistance (1651+/-369 to 1207+/-281 d
33 8% vs. 40 +/- 18%, p = NS) and a decrease in systemic vascular resistance (22 +/- 13% vs. 24 +/- 11%,
34 fidence interval, -89.4 to -3.8; P=0.03) and systemic vascular resistance (-239.3 dynes.s(-1).cm(-5);
35                     Vessel dilator decreased systemic vascular resistance 24%, pulmonary vascular res
36        However, there was also a fall in the systemic vascular resistance (-26.2+/-12.8%, P<0.005) an
37 output septic shock associated with elevated systemic vascular resistance (2C); and use of hydrocorti
38 /min; cardiac index, 6.4 +/- 0.4 L/min/min2; systemic vascular resistance, 326 +/- 107 dyne cm/s2).
39 /- 24.4 to 188.3 +/- 30.8 ml/min per m2) and systemic vascular resistance (36.8 +/- 8 to 21.9 +/- 5.5
40 17 +/- 2 versus 11 +/- 2 mm Hg; P < .05) and systemic vascular resistance (3891 +/- 379 versus 3071 +
41          NO3(-) led to greater reductions in systemic vascular resistance (-42.4+/-16.6% versus -31.8
42 ressure (57+/-4 to 84+/-2 mm Hg, P<.001) and systemic vascular resistance (813+/-113 to 1188+/-87 dyn
43 4 L/min vs 6.6 +/- 0.4 L/min, p < 0.05), but systemic vascular resistance (885 +/- 77 dyn.s/cm vs 531
44 terial pressure (69+/-8 to 93+/-4 mm Hg) and systemic vascular resistance (898+/-88 to 1443+/-72 dyne
45 ure have decreased cardiac output, increased systemic vascular resistance, abnormal diastolic functio
46 e index, diastolic blood pressure, and total systemic vascular resistance all were significantly lowe
47 h the exception of cardiac index and indexed systemic vascular resistance, all the other hepatic and
48 ease by 6 h), mean right atrial pressure and systemic vascular resistance, along with significant inc
49                 The animals' heart rates and systemic vascular resistances also did not change.
50 s attributable to either a large increase in systemic vascular resistance and a decrease in cardiac o
51 =19) had an initial considerable increase in systemic vascular resistance and a decrease in cardiac o
52 is associated with a significant increase in systemic vascular resistance and a relatively minor incr
53 e has to be dynamic to avoid the increase in systemic vascular resistance and abrupt changes in intra
54 itions, including afterload as determined by systemic vascular resistance and arterial elastance (Ea)
55 th a strict requirement for its HBD, reduces systemic vascular resistance and arterial pressure in a
56                 The use of AT(1)RB decreased systemic vascular resistance and attenuated local expres
57                                          Low systemic vascular resistance and bradycardia are also co
58                                          The systemic vascular resistance and cardiac contractility w
59                                          The systemic vascular resistance and dynamic response charac
60 nce NPY transcription and secretion, raising systemic vascular resistance and early heritable respons
61 including endothelial dysfunction, increased systemic vascular resistance and elevated systemic and p
62 trial, systolic and mean arterial pressures, systemic vascular resistance and haematocrit were not di
63 s characterized by hypotension and decreased systemic vascular resistance and impaired vascular react
64      Short-term intravenous bosentan reduced systemic vascular resistance and improved overall LV per
65  with congestive heart failure by decreasing systemic vascular resistance and improving ventricular d
66 ed arterial and central venous pressures and systemic vascular resistance and increased heart rate, c
67                      Significantly decreased systemic vascular resistance and increased left ventricu
68 ascular responders) or a smaller increase in systemic vascular resistance and no change or an increas
69 cular responders) or b) smaller increases in systemic vascular resistance and no change or an increas
70 ble individuals are unable to increase their systemic vascular resistance and plasma noradrenaline co
71 n of SQBNP, cardiac output was increased and systemic vascular resistance and pulmonary capillary wed
72 e peak effect of dipyridamole on heart rate, systemic vascular resistance and pulmonary capillary wed
73                                              Systemic vascular resistance and pulmonary vascular resi
74 ysaccharide resulted in greater increases in systemic vascular resistance and pupillary mydriasis and
75 all patients mean systemic filling pressure, systemic vascular resistance and resistance for venous r
76 nificantly higher mean arterial pressure and systemic vascular resistance and significantly lower por
77  the use of afterload reduction to stabilize systemic vascular resistance and therefore the pulmonary
78 emic reduction of Hb concentration decreased systemic vascular resistance and TO2 and increased heart
79  to both lower arterial afterload (decreased systemic vascular resistance) and higher metabolic rate.
80 ificant changes in PaO2, oxygen consumption, systemic vascular resistance, and cardiac output through
81  exhibits a reduced systolic blood pressure, systemic vascular resistance, and cardiac stroke volume.
82 greater or earlier central venous pressures, systemic vascular resistance, and changes in the BUN:Cr
83 lling pressures of the left and right heart, systemic vascular resistance, and echocardiographic left
84 rome characterized by hypotension, decreased systemic vascular resistance, and elevated cardiac index
85 irculatory state with hypotension, decreased systemic vascular resistance, and increased cardiac outp
86 ated with substantial body growth, decreased systemic vascular resistance, and increased cardiac outp
87 oxygen delivery, increases in heart rate and systemic vascular resistance, and lactic acidosis.
88                              Cardiac output, systemic vascular resistance, and mean arterial blood pr
89 reduced resting pulmonary arterial pressure, systemic vascular resistance, and pulmonary vascular res
90 ry vascular resistance, 71+/-27% increase in systemic vascular resistance, and up to a 100-fold incre
91     In the Fontan circulation, pulmonary and systemic vascular resistances are in series.
92 eded, decreased cardiac output and increased systemic vascular resistance as the most common hemodyna
93  cardiac output and stroke volume and reduce systemic vascular resistance as well as pulmonary capill
94                   Therefore, the increase in systemic vascular resistance associated with ligation of
95 iovascular state (high cardiac index and low systemic vascular resistance) associated with endotoxin
96 eased lipopolysaccharide binding protein and systemic vascular resistance below the mean (1,011 dynes
97 rdiac output (beta=0.20, P<0.0001) and lower systemic vascular resistance (beta=-0.18, P<0.0001).
98 rdiac output (beta=-0.10, P<0.05) and higher systemic vascular resistance (beta=0.08, P<0.05), wherea
99                               An increase in systemic vascular resistance between two time points did
100 njugate increased mean arterial pressure and systemic vascular resistance but did not influence cardi
101             Treatment with AT(1)RB decreased systemic vascular resistance but did not significantly i
102  significant increases in blood pressure and systemic vascular resistance but no changes in wall stre
103 put, oxygen content, oxygen consumption, and systemic vascular resistance, but were associated with s
104 creased cardiac index (by 18%) and decreased systemic vascular resistance (by 11%), serum cholesterol
105 heart rate, stroke volume, cardiac output or systemic vascular resistance (conductance) responses to
106 ), cardiac output increased 9% (P=0.04), and systemic vascular resistance decreased 18% (P<0.001).
107 fluorescent microspheres) increased 46%, and systemic vascular resistance decreased by 21% (P < .001)
108                                              Systemic vascular resistance decreased from 1413+/-453 t
109 nary capillary wedge pressure decreased 44%, systemic vascular resistance decreased significantly, an
110 nary capillary wedge pressure decreased 52%, systemic vascular resistance decreased significantly, an
111 ction fraction and cardiac output, and lower systemic vascular resistance during mental stress than p
112 ce, pulmonary artery pressure, pulmonary and systemic vascular resistances, ECG, serum cardiac enzyme
113     In the face of increased cardiac output, systemic vascular resistance fails to decline homeostati
114                             During exercise, systemic vascular resistance fell in controls and AF but
115                             During exercise, systemic vascular resistance fell, and there was no rela
116            During normoxia, L-NMMA increased systemic vascular resistance from 1,108 +/- 74 to 1,705
117                Acute hypoxia alone decreased systemic vascular resistance from 1,209 +/- 78 to 992 +/
118  +/- 18 ml (p < 0.001); and 3) a decrease in systemic vascular resistance from 1,226 +/- 481 dyn.s/cm
119 om 25 +/- 2 to 29 +/- 3 mm Hg, p < 0.05) and systemic vascular resistance (from 1,628 +/- 154 to 2,20
120 ary wedge pressure, and reduce pulmonary and systemic vascular resistance in initial clinical studies
121 e in the regulation of arterial pressure and systemic vascular resistance in this model of congestive
122 cant decreases in mean arterial pressure and systemic vascular resistance in TIVCC.
123                                    With CHF, systemic vascular resistance increased by 120%, was norm
124 P < .05) due to peripheral vasoconstriction (systemic vascular resistance increased from 644 to 1187
125             Resistance for venous return and systemic vascular resistance increased more (p = 0.019 a
126 blood pressure and pulse pressure, decreased systemic vascular resistance, increased aortic distensib
127 terial pressure (-7 mm Hg; p = 0.041) and in systemic vascular resistance index (-116 dyne.sec/cm5/m2
128 (0.43 +/- 0.17 microg/kg/min; p = 0.002) and systemic vascular resistance index (1.44 +/- 0.57 dynes/
129 e gradient (28 vs 11 cm H(2)O; P < .001) and systemic vascular resistance index (1610 vs 1384 dyn . s
130 dex (15%), and heart rate (7%) and decreased systemic vascular resistance index (21%), whereas mean a
131 d 3.06 +/- 0.79 mm Hg.m(2)/mL; P<0.0001) and systemic vascular resistance index (3116 +/- 799 versus
132  hrs that was characterized by low values of systemic vascular resistance index (p < .05) and mean ar
133 ular response characterized by a decrease in systemic vascular resistance index (p < .05), and an inc
134 etic peptide (p = 0.001; 95% CI, 0.99-1.00), systemic vascular resistance index (p < 0.001; 95% CI, 0
135 ume index (range 10.5 to 29 mL/m2), and high systemic vascular resistance index (range 1,653 to 2,997
136 ercise (P=0.02) in the sildenafil group, and systemic vascular resistance index (resting, P=0.0002; p
137 al arterial compliance (pulsatile load), and systemic vascular resistance index (steady load) were co
138 red by effective arterial elastance (Ea) and systemic vascular resistance index (SVRI), and loading s
139 re were no differences between the groups in systemic vascular resistance index (SVRI), cardiac index
140                   The aim was to investigate systemic vascular resistance index (SVRI), cardiac index
141 on of N omega-nitro-L-arginine methyl ester, systemic vascular resistance index and cardiac index ret
142       L-NMMA produced sustained increases in systemic vascular resistance index and mean arterial pre
143 , and oxygen delivery index and increases in systemic vascular resistance index and oxygen extraction
144 s in pulmonary vascular resistance index and systemic vascular resistance index at 30 to 60 mins.
145 ure, pulmonary artery occlusion pressure, or systemic vascular resistance index between animals in gr
146 lmonary artery occlusive pressure, PVRI, and systemic vascular resistance index but also in the PaO(2
147 edly increased (p < .05, synergistic effect) systemic vascular resistance index compared with endotox
148  1.6 L/min at CPAP of 5 cm H2O, p < .05) and systemic vascular resistance index decreased (2412 +/- 5
149      In septic sheep, MAP fell by ~30 mm Hg, systemic vascular resistance index decreased by ~50%, an
150 esistance index (P=0.005) increased, whereas systemic vascular resistance index decreased during exer
151 ndex increased from 3.5 to 5.4 L/min/m2, the systemic vascular resistance index decreased from 1513 t
152 th SSPH and control animals (p < .05), while systemic vascular resistance index did not change.
153 .3 L/min at CPAP of 15 cm H2O, p < .005) and systemic vascular resistance index increased (2509 +/- 7
154 n rate at normothermia, leading to increased systemic vascular resistance index not seen at normother
155                                              Systemic vascular resistance index was not associated wi
156                                              Systemic vascular resistance index was reduced (P<0.0001
157 erial compliance was lower in women, whereas systemic vascular resistance index was similar between s
158 alysis of changes in stroke volume index and systemic vascular resistance index were measured within
159 ance, Ea; total arterial compliance, Ca; and systemic vascular resistance index) in patients with LGS
160 dex, left ventricular stroke work index, and systemic vascular resistance index), metabolic parameter
161 dex, left ventricular stroke work index, and systemic vascular resistance index), metabolism (oxygen
162 cantly reduced mean arterial blood pressure, systemic vascular resistance index, and left ventricular
163 , MPAP, pulmonary artery occlusive pressure, systemic vascular resistance index, and PVRI, whereas ca
164 r N-terminal pro-B-type natriuretic peptide, systemic vascular resistance index, and stroke volume in
165 re, mean pulmonary arterial pressure (MPAP), systemic vascular resistance index, and urine output did
166                                  Heart rate, systemic vascular resistance index, left ventricular end
167 ficant differences between the two groups in systemic vascular resistance index, renal blood flow, me
168 ured mean arterial pressure, cardiac output, systemic vascular resistance index, the first derivative
169                      HS 142-1 did not change systemic vascular resistance index.
170 ted with a potentiated (p < .05) increase in systemic vascular resistance index.
171 reased mean arterial pressure, pulmonary and systemic vascular resistance indices, and arterial and m
172 rmacologic reduction in filling pressure and systemic vascular resistance leads to a reduction in the
173 d decrease in cardiac output and increase in systemic vascular resistance noted in vascular responder
174  emptying but higher blood pressure (BP) and systemic vascular resistance occur in healthy older vers
175 ia during exercise, and greater increases in systemic vascular resistance occurred with ischemia duri
176 cing aortic sinus eddy vortices and variable systemic vascular resistance on overall valve opening-cl
177 eft ventricular preload and not by increased systemic vascular resistance or heart rate.
178 between maximum TNF-alpha concentrations and systemic vascular resistance (p < .01), cardiac index (p
179 stroke volume (p < 0.017) and an increase in systemic vascular resistance (p < 0.005).
180 c output, pulmonary vascular resistance, and systemic vascular resistance (P<0.05) compared with the
181 n stroke flow was related to the decrease in systemic vascular resistance (P=0.03), increase in total
182 essure, pulmonary artery occlusion pressure, systemic vascular resistance, pulmonary vascular resista
183                                              Systemic vascular resistance; PVL: 3.7 +/- 0.1 versus 4.
184 ary arterial pressure (PAP) and pulmonary to systemic vascular resistance ratio (PVR/SVR) were 34 +/-
185 esistance, and pulmonary vascular resistance/systemic vascular resistance ratio, which indicates a se
186  caffeine decreased cardiac index, increased systemic vascular resistance, reduced portal pressure (P
187 al muscle blood flow, cardiac index (CI) and systemic vascular resistance responses to supine leg exe
188 tration for 10 weeks does not alter abnormal systemic vascular resistance, resting cardiac index, dia
189                                              Systemic vascular resistance returned toward baseline wi
190                   The ratio of pulmonary and systemic vascular resistance (Rp:Rs) was determined at b
191 lso established weight-indexed pulmonary and systemic vascular resistances (Rpi and Rsi, respectively
192  the LPS groups, all agents elevated MAP and systemic vascular resistance similarly.
193 anges in the exercise-induced cardiac index, systemic vascular resistance, stroke volume, and VO(2) i
194  initial increase in cardiac output (CO) and systemic vascular resistance (SVR) as mixed responders w
195 continuously recorded and cardiac output and systemic vascular resistance (SVR) assessed at 30-minute
196 or cocaine evokes either a large increase in systemic vascular resistance (SVR) or a smaller increase
197 was designed to reduce filling pressures and systemic vascular resistance (SVR) without inotropic the
198 lar resistance (PVR) but did not affect MAP, systemic vascular resistance (SVR), or CO.
199 c infusions have shown an opposite effect on systemic vascular resistance (SVR), possibly confounded
200 1), however, no differences were observed in systemic vascular resistance (SVR).
201 ecting mean aortic pressure (Pao) or indexed systemic vascular resistance (SVRI).
202  results in greater cardiac output and lower systemic vascular resistance than does single-chamber ve
203 vides circulatory support and an increase in systemic vascular resistance that leads to reduced vasop
204 systolic blood pressure, cardiac output, and systemic vascular resistance that were correlated with i
205 ere maintained, infusion of L-NMMA increased systemic vascular resistance (to 1,496 +/- 97 dynes-s-cm
206 ood pressure, stroke volume, cardiac output, systemic vascular resistance, total arterial compliance,
207                                  METHODS AND Systemic vascular resistance, total arterial compliance,
208  extraction above baseline, and decreases of systemic vascular resistance, total Hb, total solids, ar
209 e by augmenting cardiac indices, leaving the systemic vascular resistance unaffected.
210 ia the COX-2 pathway can alter pulmonary and systemic vascular resistance was investigated, and the e
211 iac index was significantly higher and total systemic vascular resistance was lower in all groups of
212 ere increased; b) plasma lactate was higher, systemic vascular resistance was lower, but ileal mucosa
213  did not increase above baseline values, and systemic vascular resistance was unchanged following adm
214 /-0.6 and 3.7+/-0.4 L/min, and pulmonary and systemic vascular resistance were 312+/-134 and 2006+/-3
215 enous pressure gradient, cardiac output, and systemic vascular resistance were made at baseline and a
216 ate, pulmonary capillary wedge pressure, and systemic vascular resistance were measured throughout th
217 .01+/-0.26 L/min; P<0.001); the decreases in systemic vascular resistance were not different.
218 y correlated with mean arterial pressure and systemic vascular resistance, whereas levels of ADMA cor
219 anaesthesia is caused by a rapid decrease in systemic vascular resistance, which makes alpha-agonists
220 tility, also induced tachycardia and loss of systemic vascular resistance, which were not seen with l
221 ate by increasing mean arterial pressure and systemic vascular resistance while decreasing cardiac in
222 h left and right heart filling pressures and systemic vascular resistance, while increasing cardiac a
223 -adrenergic mechanisms may serve to increase systemic vascular resistance with ageing, and that the e
224 dynamic response patterns: a) an increase in systemic vascular resistance with cardiac depression (va
225 y capillary wedge pressure and pulmonary and systemic vascular resistances, with no change in heart r
226 hock) raised arterial pressure by increasing systemic vascular resistance without a significant prefe
227                      ACE inhibitors decrease systemic vascular resistance without increasing heart ra

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