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1 brovascular counter-regulation of changes in arterial pressure.
2 dant increases of resting metabolic rate and arterial pressure.
3 th radiotelemetry devices for recording mean arterial pressure.
4 ressed partly by increases in heart rate and arterial pressure.
5 this exposure to a 5 mm Hg reduction in mean arterial pressure.
6 adjusted for age, body mass index, and mean arterial pressure.
7 voke a pressor reflex known to increase mean arterial pressure.
8 Mean pulmonary arterial pressure.
9 vides prognostic utility beyond that of mean arterial pressure.
10 c BP, diastolic BP, pulse pressure, and mean arterial pressure.
11 rdiovascular outcomes, independently of mean arterial pressure.
12 d a norepinephrine infusion to maintain mean arterial pressure.
13 brain hypoperfusion during acute increase in arterial pressure.
14 n II, and resulted in better preservation of arterial pressure.
15 Neither candesartan nor CAP affected arterial pressure.
16 n 21% O(2) ), to selectively lower pulmonary arterial pressure.
17 67 dynes; p < 0.001) with no effects on mean arterial pressure.
18 echocardiographic cardiac index and the mean arterial pressure.
19 ricular stroke volume without affecting mean arterial pressure.
20 affected by baseline serum lactate and mean arterial pressure.
21 ean arterial pressure was above optimal mean arterial pressure.
22 d this correlated with post-brain death mean arterial pressures.
23 st circumference (-1.1 to -1.9 cm), and mean arterial pressure (0.0 to -1.1 mm Hg) at 6 months and Fr
24 8.7, -5.1]; p(group) < 0.0001), similar mean arterial pressure (-1.1 mm Hg [95% confidence limit, -2.
25 0+/-4 versus 6+/-3 mm Hg; P=0.02), pulmonary arterial pressure (22+/-8 versus 11+/-4 mm Hg; P=0.0001)
26 ation, terlipressin decreased mean pulmonary arterial pressure (-6.5 +/- 1.8 mm Hg; p = 0.005) and te
27 7 +/- 451 mL; p = 0.005), and mean pulmonary arterial pressure (-7 +/- 1 mm Hg; p < 0.001) and increa
28 7 mm Hg; 95% CI, -25 to -8; p < 0.001), mean arterial pressure (-7 mm Hg; 95% CI, -12 to -1; p = 0.02
29 : 0.4, 1.7; p = 0.001), 0.8-mmHg higher mean arterial pressure (95% CI: 0.2, 1.4; p = 0.01), and no s
30 nd COMACARE (Carbon Dioxide, Oxygen and Mean Arterial Pressure After Cardiac Arrest and Resuscitation
32 performed a comprehensive time-weighted mean arterial pressure analysis (time-weighted-average-mean a
33 resulted in a 37 mmHg reduction in systolic arterial pressure and 19% inhibition of angiotensin conv
34 sin II caused a significant increase in mean arterial pressure and a rapid reduction in catecholamine
35 Antagonism of P2X3 receptors also reduces arterial pressure and basal sympathetic activity and nor
37 elation was observed between changes in mean arterial pressure and cardiac index (r = 0.035, p = 0.79
38 assessed for each time-weighted-average-mean arterial pressure and cumulative-time-below mean arteria
39 ressure analysis (time-weighted-average-mean arterial pressure and cumulative-time-below various mean
41 s, we demonstrate that ELA and 3 both reduce arterial pressure and exert positive inotropic effects o
44 ucted a model on the basis of proximal renal arterial pressure and flow velocity measurements that pr
45 urons also resulted in a significant fall in arterial pressure and heart rate that was similar in mag
46 and the hypoxia-induced CR (O(2) -CR), mean arterial pressure and heart rate were significantly grea
47 sociation between time-weighted-average-mean arterial pressure and ICU-mortality for each threshold r
48 in RN-NSC-grafted rats reduced resting mean arterial pressure and increased heart rate in all but 2
51 MRI, in combination with measurement of peak arterial pressure and MRI-derived timing of valvular eve
55 terial baroreflex gain, and provoked smaller arterial pressure and R-R interval fluctuations, which w
56 re no differences between groups in the mean arterial pressure and R-R interval responses to non-burs
58 ncreased risk for incident CVD, whereas mean arterial pressure and relative wave reflection (correlat
60 o-obliteration leading to elevated pulmonary arterial pressure and resistance, right ventricular dysf
61 tion, the steady-state relationships between arterial pressure and sodium excretion, a correlation th
63 adratic) association between the lowest mean arterial pressure and the primary outcome of myocardial
64 minute; P<0.01) despite a reduction in mean arterial pressure and was inversely related to pulse pre
65 strongly correlated with pulse and systolic arterial pressures and with total arterial stiffness, re
66 activity index and identify the optimal mean arterial pressure, and 3) assess the relationship betwee
67 D with forward pressure wave amplitude, mean arterial pressure, and global reflection coefficient der
68 tonically suppresses splanchnic SNA (SSNA), arterial pressure, and heart rate via projections to the
69 lla (RVLM) lower sympathetic nerve activity, arterial pressure, and heart rate, or when administered
70 percentage of total blood volume (TBV), mean arterial pressure, and heart rate, which were recorded a
71 iomarkers, such as WBC, oxygen content, mean arterial pressure, and heart rate, yielded estimation ac
72 ldosterone improved 5-day survival, invasive arterial pressure, and in vivo and ex vivo arterial resp
73 e, uses shock index as a substitute for mean arterial pressure, and incorporates serum lactate as a b
75 pressure, cerebral perfusion pressure, mean arterial pressure, and jugular venous bulb oxygen satura
76 cipient age, body mass index, mean pulmonary arterial pressure, and pretransplant diagnosis, higher E
77 s subjects, right atrial pressure, pulmonary arterial pressure, and pulmonary capillary wedge pressur
78 ood pressure, diastolic blood pressure, mean arterial pressure, and pulse pressure from the Internati
80 s to describe changes in cardiac index, mean arterial pressure, and their relationship to other indic
84 ts during vasoactive drug-induced changes in arterial pressure assessed at the internal carotid and v
85 Every 10 mmHg drop from baseline in mean arterial pressure associated with a 3% increase in ische
87 e blood volume, subsequent titration of mean arterial pressure at 35 mm Hg), anesthetized and instrum
89 guidelines, which recommend maintaining mean arterial pressure at 85 to 90mm Hg for a week after spin
90 nd point was a response with respect to mean arterial pressure at hour 3 after the start of infusion,
91 on, norepinephrine titrated to maintain mean arterial pressure at preshock values, mechanical ventila
92 imates and invasive measurement of pulmonary arterial pressure at rest and peak exercise were simulta
93 ic pressure was calculated as 0.9 x systolic arterial pressure at the carotid, femoral, and radial ar
94 oups in the median cumulative time with mean arterial pressure below 60 mm Hg (7 vs 7 minutes; differ
95 erial pressure: for 1 mm Hg decrease in mean arterial pressure below 75, 70, 65, 60, and 55 mm Hg, th
96 systolic BP (beta=-4.11; P=2.8x10(-4)), mean arterial pressure (beta=-3.50; P=8.9x10(-6)), and reduce
97 , consisting of age, oxygen saturation, mean arterial pressure, blood urea nitrogen, C-Reactive prote
100 an arterial pressure approached optimal mean arterial pressure, brain tissue oxygenation increased (p
101 MCS devices increased forward blood flow and arterial pressure but other effects varied among devices
105 ut no effect on macrocirculatory parameters (arterial pressure, cardiac index, heart rate, and pulse
107 ood pressure, diastolic blood pressure, mean arterial pressure, carotid intima-media thickness and bo
108 s: preflight, late mission and landing day.) Arterial pressure changed systematically from preflight
110 uencies and probabilities increased, even as arterial pressure climbed to new levels); or altered pul
111 NOS3 and GUCY1A3 expression and reduced mean arterial pressure, combined them into a genetic score, a
112 he 25th percentile (78 mm Hg) of lowest mean arterial pressure compared with at the median of 87 mm H
113 than the intact group (2-month fall in mean arterial pressure: control-intact, -10 +/- 1 mm Hg; cont
114 cardiographic measures of systolic pulmonary arterial pressure correlated reasonably well with invasi
116 degree of hemodynamic instability (mean [SD] arterial pressure decreases of 25 [1] and 41 [11] mm Hg,
118 ve cyclooxygenase-2 inhibitor, abolished the arterial pressure difference between the knockout and co
121 l mice, Pkd1 knockout mice exhibited reduced arterial pressure during high salt intake; this associat
122 y two and fivefold, respectively, normalized arterial pressure during LVR, and lowered plasma lactate
124 C) activation and reflexively increases mean arterial pressure; endomorphin release is also increased
126 isodes of hypotension were common, with mean arterial pressure falling by a median of 22 mmHg (interq
129 CR, or HS/CR+MC-2 (HS = 40% of baseline mean arterial pressure for 60 minutes; CR = return of shed bl
133 rom 351 +/- 55 to 182 +/- 67 mL/min and mean arterial pressure from 96.7 +/- 18.2 to 41.5 +/- 4.6 mm
134 o extracorporeal membrane oxygenation, lower arterial pressure, fungal pneumonia, and advancing age.
135 5-year-old female uni-x and sham sheep, mean arterial pressure, glomerular filtration rate, and renal
136 ding PTA versus renal stent placement, intra-arterial pressure gradient greater than 10%, diastolic B
137 tropic Score greater than 50 to reach a mean arterial pressure greater than 65 mm Hg despite adequate
138 uded the following physiologic targets: mean arterial pressure greater than 70 mm Hg, cerebral perfus
139 than or equal to 20 mm Hg, decrease in mean arterial pressure greater than or equal to 10 mm Hg, dec
140 s the need for vasopressors to maintain mean arterial pressure greater than or equal to 65 mm Hg and
141 sistent with POPH (defined as mean pulmonary arterial pressure >25 mm Hg and pulmonary vascular resis
143 d treatment with vasopressors targeting mean arterial pressure (>/=65 mm Hg) and blood transfusion (f
144 ood flow in response to transient changes in arterial pressure has been used to assess dynamic CA.
145 s associated with incident CVD, whereas mean arterial pressure (hazard ratio, 1.10; 95% confidence in
146 objective physical variables (including mean arterial pressure, heart rate, respiratory rate, and oxy
147 PDE9-I also produced progressive falls in arterial pressure (HF: p < 0.001), atrial pressure (Norm
148 tion (HR: 23.2; P = 0.01), and baseline mean arterial pressure (HR: 0.92; P = 0.01) were found to be
150 atory modulation of sympathetic activity and arterial pressure in both normotensive and CIH hypertens
151 tensive and CIH hypertensive rats, but basal arterial pressure in CIH rats remained higher compared t
152 Iron deficiency augments hypoxic pulmonary arterial pressure in healthy individuals and exacerbates
153 ale: Exogenous angiotensin II increases mean arterial pressure in patients with catecholamine-resista
155 r agonist), caused a graded increase in mean arterial pressure in rats with sinoaortic denervation an
156 asal blood pressure and acute change in mean arterial pressure in response to angiotensin II (Ang II)
157 erence in the primary outcome of 6-hour mean arterial pressure in septic shock patients receiving vas
158 ained by transcranial Doppler sonography and arterial pressure in the radial artery was obtained by t
159 r 1 (BLT1) receptor with CP-105,696, reduced arterial pressure in the SHR compared to the normotensiv
164 investigated whether reductions in pulmonary arterial pressure influenced sympathetic outflow and bar
166 The Intraoperative Norepinephrine to Control Arterial Pressure (INPRESS) study was a multicenter, ran
167 d perfusion within proximity of optimal mean arterial pressure is associated with increased brain tis
172 pital location, era, systolic pressure, mean arterial pressure, lactate, bundle compliance, amount of
173 tcomes included 24-hour survival rates, mean arterial pressure, lactate, hemoglobin, and estimated in
174 Exclusion criteria for both groups were mean arterial pressure less than 60 mm Hg, contraindications
175 nificant associations only remained for mean arterial pressure less than 65 mm Hg (odds ratio, 1.07;
176 tality included: a single occurrence of mean arterial pressure less than 65 mm Hg (p = 0.0051) or sys
178 itivity analyses based on every hour of mean arterial pressure less than 80 mm Hg and any mean arteri
180 sure reactivity index can yield optimal mean arterial pressure, lower and upper limit of autoregulati
181 ty index-based determination of optimal mean arterial pressure, lower and upper limit of autoregulati
183 oach, we demonstrate that reducing pulmonary arterial pressure lowers basal MSNA in healthy humans.
184 (systolic blood pressure </=90 mm Hg or mean arterial pressure </=65 mm Hg) presenting to the emergen
185 ndomized to strict or usual BP control (mean arterial pressure </=92 mmHg or 102-107 mmHg, respective
186 dynamic deterioration with an intrinsic mean arterial pressure <60 mm Hg during a sustained episode.
187 albumin <2.5 g/dL, heart rate >90 bpm, mean arterial pressure <60 mmHg, white blood cell count >/=15
190 es to identify the relationship between mean arterial pressure (MAP) and cerebral blood vessels' diam
191 or reflex (EPR) is defined by a rise in mean arterial pressure (MAP) and heart rate (HR) in response
192 -wide gene-smoking interaction study of mean arterial pressure (MAP) and pulse pressure (PP) in 129 9
196 is study aimed to determine the optimal mean arterial pressure (MAP) in patients with AMI and shock a
197 vels of estradiol-17beta (E2) increases mean arterial pressure (MAP) in young female Sprague-Dawley (
198 nt of CA during steady-state changes in mean arterial pressure (MAP) induced by intravenous infusion
200 BP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) were significantly (P < 0.05) re
205 ood pressure, diastolic blood pressure, mean arterial pressure (MAP)], brachial artery blood flow ( Q
206 dural increase of median SBP (+11%) and mean arterial pressure (MAP, +10%, both p < 0.001), and a uni
208 ension (PH) is diagnosed by a mean pulmonary arterial pressure (mPAP) value of at least 25 mm Hg duri
209 that showed correlation with mean pulmonary arterial pressure (mPAP) were used to create a regressio
210 class (WHO FC); and change in mean pulmonary arterial pressure (mPAP), pulmonary vascular resistance
211 ression of Kv1.5 channels), we measured mean arterial pressure, myocardial blood flow, myocardial tis
213 oventricular CMT-3 attenuated increased mean arterial pressure, normalized sympathetic activity, and
214 o, 2.71; 95% CI, 1.67-4.39; p < 0.001), mean arterial pressure (odds ratio, 0.979; 95% CI, 0.963-0.99
215 agic shock by blood withdrawn until the mean arterial pressure of 30 mm Hg and maintained at this pre
217 a vasopressor requirement to maintain a mean arterial pressure of 65 mm Hg or greater and serum lacta
220 These data suggest that maintaining a mean arterial pressure of greater than 65 mm Hg may be a reas
221 ension was defined as a decrease in the mean arterial pressure of greater than or equal to 15% compar
222 by a progressive elevation in mean pulmonary arterial pressure, often leading to right ventricular fa
223 o assess the association between lowest mean arterial pressure on each intensive care day, considered
224 ltivariate linear regression models for mean arterial pressure or SVRI in patients with severe malari
226 atinine, bilirubin or albumin, baseline mean arterial pressure, or study design, size or time period.
227 on and magnitude of clinically observed mean arterial pressure outside optimal mean arterial blood pr
228 1) and a two-fold increase in mean pulmonary arterial pressure (p < 0.0001) compared with baseline.
229 Pulmonary embolism increased mean pulmonary arterial pressure (p < 0.0001), pulmonary vascular resis
230 s (p < 0.05), cardiac index (p < 0.05), mean arterial pressure (p < 0.05), PaO2/FIO2 (p < 0.05), and
231 as low recruiters experienced lower systolic arterial pressure (P = 0.008).Conclusions: A single-brea
234 ounts of hypotension (defined by lowest mean arterial pressures per day) were strongly associated wit
235 ated that independent of differences in mean arterial pressure, pH and blood viscosity, race accounts
236 bserved that despite a threefold increase in arterial pressure power <0.03 Hz with oscillatory LBP, t
238 use, blood pressure medication use, and mean arterial pressure, PP quartile was still associated with
240 an+/-SD, 8.3+/-2.8 per subject) of pulmonary arterial pressure, pulmonary arterial wedge pressure and
242 y correlated with decreases in the diastolic arterial pressure (r = 0.92) and to a lesser extent with
243 udy was to examine the effect of RDN on mean arterial pressure, renal function, and the reflex respon
244 n Earth with electrocardiogram, non-invasive arterial pressure, respiratory carbon dioxide concentrat
245 ctrocardiogram, finger photoplethysmographic arterial pressure, respiratory carbon dioxide levels, ti
248 eat fluid bolus based solely on lack of mean arterial pressure response to the initial fluid, since t
251 herapy in the improvement of 6MWD, pulmonary arterial pressure, right atrial pressure, cardiac index
253 Factors associated with higher cIMT and mean arterial pressure SD-scores were HD group, higher ultraf
254 inephrine required to maintain a target mean arterial pressure; secondary outcomes included hemodynam
256 atment prevented the further decline in mean arterial pressure, substantially reduced heart rate and
259 in maximum negative dP/dt (dP/dt(Min)), mean arterial pressure, systolic pressure, diastolic pressure
261 als are needed to determine the optimal mean arterial pressure-targets in this patient population.
262 the lactic acid-mediated reflex increase in arterial pressure that is MOR stimulation-independent an
264 rial pressure and cumulative-time-below mean arterial pressure threshold (55, 60, 65, 70, and 75 mm H
265 ity and duration of hypotension below a mean arterial pressure threshold and cumulative-time-below is
267 ssure and cumulative-time-below various mean arterial pressure-thresholds) during the first 24-hours
268 ctrocardiogram, finger photoplethysmographic arterial pressure, tidal carbon dioxide concentrations a
269 ctrocardiogram, finger photoplethysmographic arterial pressure, tidal volume, respiratory carbon diox
271 ters, grafting RN-NSCs restored resting mean arterial pressure to normal levels and remarkably allevi
273 ents with grade A TR signals, mean pulmonary arterial pressure-to-workload ratio at a threshold of 1.
274 reduction of right ventricular and pulmonary arterial pressures, toward normal levels of right-side p
275 roteinuria were repeat transplantation, mean arterial pressure, transplant glomerulopathy, microcircu
277 increased noradrenaline dose to elevate mean arterial pressure up to 85-90 mm Hg before collecting a
279 QRS-gated DPD demonstrated higher pulmonary arterial pressures versus isolated postcapillary pulmona
280 nce (FVC; Doppler ultrasound, brachial intra-arterial pressure via catheter) to local intra-arterial
284 ionship did not persist when the actual mean arterial pressure was above optimal mean arterial pressu
286 LT1) receptors were blocked with CP-105,696, arterial pressure was reduced in the SHR compared to the
289 mathematical model for long-term control of arterial pressure was the model of Guyton and Coleman; r
290 aneous vascular conductance (CVC = flux/mean arterial pressure) was expressed as a change from baseli
291 g pump controller parameters and noninvasive arterial pressure waveforms, central aortic pressure, ou
295 tmax, systolic, diastolic, and pulse femoral arterial pressure were obtained from the pressure wavefo
296 olume, cardiac output and reductions in mean arterial pressure were similar between age groups and co
298 ficant increases (P < 0.05; n = 7-8) in mean arterial pressure, which were generally accompanied by s
300 one of the other indices including pulmonary arterial pressure (WMD: -0.97 mmHg, 95%CI: -4.39, 2.44,