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1 d by hypernatremia or elevated AngII but not hypovolemia.
2 ic reflex vasoconstriction was stimulated by hypovolemia.
3 a, fever, leukocytosis, hypoalbuminemia, and hypovolemia.
4 ic shock caused by myocardial depression and hypovolemia.
5 -mediated amplification of histamine-induced hypovolemia.
6 suggesting greater ability to defend against hypovolemia.
7 ith acute tubular necrosis in the absence of hypovolemia.
8  than 2 mmol/L (>18 mg/dL) in the absence of hypovolemia.
9 ythrocytes in the microcirculation, not from hypovolemia.
10  loading in the critically ill with presumed hypovolemia.
11 onditions of severe hemodilution followed by hypovolemia.
12 w-sodium and high-aldosterone states such as hypovolemia.
13 on, CSF leak, low pressure headache, and CSF hypovolemia.
14 e useful to reduce organ injury after severe hypovolemia.
15 tes in an adult porcine model of hemorrhagic hypovolemia.
16  this pediatric porcine model of hemorrhagic hypovolemia.
17 of dependent extremities with redistributive hypovolemia.
18 ng orthostatic stress after HDTBR than after hypovolemia.
19 5) after HDTBR and by 18+/-8% (P<0.05) after hypovolemia.
20 is not seen with equivalent degrees of acute hypovolemia.
21 to saline infusion to correct the underlying hypovolemia.
22 cardiac disease (9%), drug effects (9%), and hypovolemia (7%).
23  function developing unexplained ARF without hypovolemia after administration of vancomycin without c
24 ction: P < 0.01) were higher during moderate hypovolemia after ketamine vs. placebo administration (P
25 e and heart rate were higher during moderate hypovolemia after ketamine vs. placebo administration.
26 uring orthostatic stress after bed rest than hypovolemia alone, potentially contributing to orthostat
27 le was decreased after HDTBR; however, after hypovolemia alone, the curve was identical, with no chan
28  to head-down tilt bed rest (HDTBR) or acute hypovolemia alone.
29                                     However, hypovolemia also elicited changes in capillary volume, s
30                        A dynamic orthostatic hypovolemia and alpha1-adrenoreceptor hypersensitivity h
31 tolerance after bed rest is characterized by hypovolemia and an excessive reduction in stroke volume
32 d can lead to hypochloremia and subsequently hypovolemia and decreased glomerular filtration rate.
33 ry state of cirrhosis that leads to relative hypovolemia and decreased renal blood flow, patients wit
34 ra were recorded every 10 mins during serial hypovolemia and during a 30-min recovery period.
35 ginine vasopressin (AVP) are elevated during hypovolemia and during cardiac stress.
36 achycardia syndrome (POTS) to counteract the hypovolemia and elevated plasma norepinephrine that cont
37 aria and metabolic acidosis have evidence of hypovolemia and evidence of cardiac dysfunction.
38 er warning signs of severe dengue, including hypovolemia and fluid accumulation, were associated with
39 d characterized by neonatal life-threatening hypovolemia and hyperkalemia.
40 o-baboon kidney transplantation, episodes of hypovolemia and hypotension from an unexplained mechanis
41                                      Central hypovolemia and impending cardiovascular collapse were i
42 iated with an increased tolerance to central hypovolemia and increased levels of circulating norepine
43 ion was associated with progressive signs of hypovolemia and increased plasma levels of interleukin-6
44 s associated with IOT are principally due to hypovolemia and loss of adequate lower-extremity vascula
45 dy was, therefore, to explore the effects of hypovolemia and pain on tissue oxygen saturation (measur
46 easurement sites) and perfusion index during hypovolemia and pain than during normovolemia and pain.
47         Fatal cases had features of relative hypovolemia and reduced cardiac index reserve.
48           Development of severe IgE-mediated hypovolemia and shock required VE-restricted ABL1 expres
49                   Enhanced postural thoracic hypovolemia and splanchnic hypervolemia are associated w
50 al fainting is related to excessive thoracic hypovolemia and splanchnic hypervolemia during orthostas
51 criteria to accurately capture patients with hypovolemia and tissue hypoperfusion who are most likely
52 itral valve (MV) occurring in the setting of hypovolemia and/or inotrope usage.
53 ., pulmonary embolism, cardiac tamponade, or hypovolemia, and signal the return of ventricular contra
54 ropsy and histology ruled out hemorrhage and hypovolemia as causes of death.
55               Many diseases, such as sepsis, hypovolemia, atrial fibrillation, congestive heart failu
56 fluid status to avoid volume overload and/or hypovolemia, avoiding hypo- and/or hypertension, treatin
57 ne do not suppress CRH gene activation after hypovolemia, but instead determine the prestress lower l
58 tion suppresses CRH gene transcription after hypovolemia, but not the preproenkephalin and c-fos mRNA
59 tate levels at admission without evidence of hypovolemia, cardiogenic failure, or vasodilatory shock.
60                                              Hypovolemia caused an increase in flow heterogeneity in
61     In experimental animals after 4 hours of hypovolemia, corticosterone dropped to 308.9 ng/mL (P =
62 nsion, low CSF pressure, low CSF volume, CSF hypovolemia, CSF hypovolaemia, spontaneous spinal CSF le
63 L/kg/min led to the following changes during hypovolemia: decreases in mean arterial blood pressure (
64 appropriately activating the CRH gene during hypovolemia, does not mediate the suppressed gene respon
65 dizziness is required to clinically diagnose hypovolemia due to blood loss, although these findings a
66 sufficient fluid intake and is distinct from hypovolemia due to excess fluid losses.
67  illness induces capillary leak resulting in hypovolemia, edema, tissue dysoxia, organ failure and ev
68  increased infection risk, cold diuresis and hypovolemia, electrolyte disorders, insulin resistance,
69 of which include hyponatremia, hyperkalemia, hypovolemia, elevated plasma renin activity, and sometim
70                         Safety outcomes were hypovolemia, fractures, falls, genital infections, diabe
71 le diameter was 32 mm (95% CI, 29-35) in the hypovolemia group, 29 mm (95% CI, 26-32) in the hyperkal
72  resuscitation from cardiac arrest caused by hypovolemia, hyperkalemia, and primary arrhythmia.
73  resuscitation from cardiac arrest caused by hypovolemia, hyperkalemia, or primary arrhythmia (i.e.,
74  assigned to cardiac arrest caused by either hypovolemia, hyperkalemia, or primary arrhythmia.
75 d renal loss of NaCl, K+, and water, causing hypovolemia, hypokalemia, and polyuria.
76  also common, including sodium depletion and hypovolemia, hypophosphatemia and hypomagnesemia.
77 namic instability during progressive central hypovolemia in humans.
78                             The treatment of hypovolemia in patients with non-cerebral trauma should
79 ex are proposed as early indirect markers of hypovolemia in trauma patients.
80 saturation and perfusion index as markers of hypovolemia in trauma patients.
81 sly assessed in a pediatric porcine model of hypovolemia induced by hemorrhage.
82 M NaCl, in addition to water, in response to hypovolemia induced by subcutaneous injection of 30% pol
83                   Of the 320 cases, 153 were hypovolemia-induced AKI (48%), 93 were HRS-AKI (29%), 39
84 d by 20+/-4% after HDTBR and by 7+/-2% after hypovolemia (interaction P<0.001).
85                                              Hypovolemia is associated with increased sympathetic ner
86                                Intravascular hypovolemia is common at the time of anesthesia inductio
87 rdial contractility or induce hypotension if hypovolemia is corrected, and preliminary evidence sugge
88                               Both HDTBR and hypovolemia led to a similar reduction in plasma volume.
89 n and perfusion index are further reduced by hypovolemia (lower body negative pressure, -60 mm Hg).
90         The etiologies of shock unrelated to hypovolemia must also be investigated.
91 ents, its effect on the indirect measures of hypovolemia needs to be clarified.
92 RBC velocity in septic shock, heart failure, hypovolemia, obstructive shock, and hemodilution and thu
93  recognition of complicating physiology (eg, hypovolemia or cardiogenic shock), while invasive hemody
94 ption or maximal K+ secretion in response to hypovolemia or hyperkalemia, respectively.
95 ation from the scaling relation may indicate hypovolemia or hypervolemia and aid diagnosis.
96 ndogenous generation of Ang II during either hypovolemia or hypotension.
97 bolus of 10 ml per kilogram in patients with hypovolemia or no bolus in patients with normovolemia, f
98  - areas previously shown to be activated by hypovolemia or peripheral angiotensin.
99 PEG; a colloid that produces non-hypotensive hypovolemia) or isoproterenol (hypotensive agent).
100  Hg) without increasing risk of hypotension, hypovolemia, or other serious adverse events, irrespecti
101 ossible underlying pathophysiologies include hypovolemia, partial dysautonomia, or a primary hyperadr
102 ce of a dry axilla supports the diagnosis of hypovolemia (positive likelihood ratio, 2.8; 95% CI, 1.4
103 by drinking hypertonic saline) and sustained hypovolemia (produced by subcutaneous injections of poly
104                                 Irreversible hypovolemia remains a major clinical problem.
105 aC persisted at day 5 in nephrotic mice when hypovolemia resolved and steady-state was reached.
106 identified as massive pulmonary embolism and hypovolemia, respectively.
107                 Treatment with L-NAME during hypovolemia resulted in increased log low-frequency hear
108   After 50% hemorrhage followed by 1 hour of hypovolemia resuscitation with 35% of blood volume using
109 d finger perfusion index were reduced during hypovolemia/sham compared with normovolemia/sham.
110  activation in a setting of left ventricular hypovolemia stimulates ventricular afferents that trigge
111 analysis, the right ventricle was larger for hypovolemia than for primary arrhythmia (p < 0.001).
112 ot been studied with the concomitant central hypovolemia that occurs during haemorrhage.
113                      Among ICU patients with hypovolemia, the use of colloids vs crystalloids did not
114 efill (2C); for septic shock associated with hypovolemia, the use of crystalloids or albumin to deliv
115 tabolic acidosis is frequently attributed to hypovolemia, tissue hypoperfusion, and lactic acidosis.
116 nduced tissue hypoperfusion and suspicion of hypovolemia to achieve a minimum of 30 mL/kg of crystall
117 toire of putative clinical applications from hypovolemia to Alzheimer's disease.
118 ting to emergency departments with suspected hypovolemia, usually due to vomiting, diarrhea, or decre
119  rats with APX also was observed when marked hypovolemia was induced by s.c. administration of a hype
120                                      Central hypovolemia was induced with lower body negative pressur
121                                              Hypovolemia was maintained for 60 mins in test animals,
122 85 mL/kg) every 10 mins until 30% cumulative hypovolemia was reached.
123                                              Hypovolemia with reduced oxygen delivery and microvascul
124 ase in arterial pressure without evidence of hypovolemia, with a systolic pressure lower than 90 mm H

 
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