ライフサイエンスコーパス: hypovolemia

1 than 2 mmol/L (>18 mg/dL) in the absence of hypovolemia.

2 ythrocytes in the microcirculation, not from hypovolemia.

3 loading in the critically ill with presumed hypovolemia.

4 onditions of severe hemodilution followed by hypovolemia.

5 w-sodium and high-aldosterone states such as hypovolemia.

6 on, CSF leak, low pressure headache, and CSF hypovolemia.

7 e useful to reduce organ injury after severe hypovolemia.

8 tes in an adult porcine model of hemorrhagic hypovolemia.

9 this pediatric porcine model of hemorrhagic hypovolemia.

10 of dependent extremities with redistributive hypovolemia.

11 ng orthostatic stress after HDTBR than after hypovolemia.

12 5) after HDTBR and by 18+/-8% (P<0.05) after hypovolemia.

13 is not seen with equivalent degrees of acute hypovolemia.

14 ith acute tubular necrosis in the absence of hypovolemia.

15 to saline infusion to correct the underlying hypovolemia.

16 ic reflex vasoconstriction was stimulated by hypovolemia.

17 a, fever, leukocytosis, hypoalbuminemia, and hypovolemia.

18 ic shock caused by myocardial depression and hypovolemia.

19 function developing unexplained ARF without hypovolemia after administration of vancomycin without c

20 uring orthostatic stress after bed rest than hypovolemia alone, potentially contributing to orthostat

21 le was decreased after HDTBR; however, after hypovolemia alone, the curve was identical, with no chan

22 to head-down tilt bed rest (HDTBR) or acute hypovolemia alone.

23 However, hypovolemia also elicited changes in capillary volume, s

24 A dynamic orthostatic hypovolemia and alpha1-adrenoreceptor hypersensitivity h

25 tolerance after bed rest is characterized by hypovolemia and an excessive reduction in stroke volume

26 d can lead to hypochloremia and subsequently hypovolemia and decreased glomerular filtration rate.

27 ry state of cirrhosis that leads to relative hypovolemia and decreased renal blood flow, patients wit

28 ra were recorded every 10 mins during serial hypovolemia and during a 30-min recovery period.

29 ginine vasopressin (AVP) are elevated during hypovolemia and during cardiac stress.

30 aria and metabolic acidosis have evidence of hypovolemia and evidence of cardiac dysfunction.

31 d characterized by neonatal life-threatening hypovolemia and hyperkalemia.

32 Central hypovolemia and impending cardiovascular collapse were i

33 ion was associated with progressive signs of hypovolemia and increased plasma levels of interleukin-6

34 s associated with IOT are principally due to hypovolemia and loss of adequate lower-extremity vascula

35 dy was, therefore, to explore the effects of hypovolemia and pain on tissue oxygen saturation (measur

36 easurement sites) and perfusion index during hypovolemia and pain than during normovolemia and pain.

37 Development of severe IgE-mediated hypovolemia and shock required VE-restricted ABL1 expres

38 Enhanced postural thoracic hypovolemia and splanchnic hypervolemia are associated w

39 al fainting is related to excessive thoracic hypovolemia and splanchnic hypervolemia during orthostas

40 criteria to accurately capture patients with hypovolemia and tissue hypoperfusion who are most likely

41 ., pulmonary embolism, cardiac tamponade, or hypovolemia, and signal the return of ventricular contra

42 ropsy and histology ruled out hemorrhage and hypovolemia as causes of death.

43 Many diseases, such as sepsis, hypovolemia, atrial fibrillation, congestive heart failu

44 ne do not suppress CRH gene activation after hypovolemia, but instead determine the prestress lower l

45 tion suppresses CRH gene transcription after hypovolemia, but not the preproenkephalin and c-fos mRNA

46 tate levels at admission without evidence of hypovolemia, cardiogenic failure, or vasodilatory shock.

47 Hypovolemia caused an increase in flow heterogeneity in

48 In experimental animals after 4 hours of hypovolemia, corticosterone dropped to 308.9 ng/mL (P =

49 L/kg/min led to the following changes during hypovolemia: decreases in mean arterial blood pressure (

50 appropriately activating the CRH gene during hypovolemia, does not mediate the suppressed gene respon

51 dizziness is required to clinically diagnose hypovolemia due to blood loss, although these findings a

52 sufficient fluid intake and is distinct from hypovolemia due to excess fluid losses.

53 increased infection risk, cold diuresis and hypovolemia, electrolyte disorders, insulin resistance,

54 of which include hyponatremia, hyperkalemia, hypovolemia, elevated plasma renin activity, and sometim

55 le diameter was 32 mm (95% CI, 29-35) in the hypovolemia group, 29 mm (95% CI, 26-32) in the hyperkal

56 resuscitation from cardiac arrest caused by hypovolemia, hyperkalemia, and primary arrhythmia.

57 resuscitation from cardiac arrest caused by hypovolemia, hyperkalemia, or primary arrhythmia (i.e.,

58 assigned to cardiac arrest caused by either hypovolemia, hyperkalemia, or primary arrhythmia.

59 d renal loss of NaCl, K+, and water, causing hypovolemia, hypokalemia, and polyuria.

60 also common, including sodium depletion and hypovolemia, hypophosphatemia and hypomagnesemia.

61 namic instability during progressive central hypovolemia in humans.

62 The treatment of hypovolemia in patients with non-cerebral trauma should

63 ex are proposed as early indirect markers of hypovolemia in trauma patients.

64 saturation and perfusion index as markers of hypovolemia in trauma patients.

65 sly assessed in a pediatric porcine model of hypovolemia induced by hemorrhage.

66 M NaCl, in addition to water, in response to hypovolemia induced by subcutaneous injection of 30% pol

67 d by 20+/-4% after HDTBR and by 7+/-2% after hypovolemia (interaction P<0.001).

68 Hypovolemia is associated with increased sympathetic ner

69 Intravascular hypovolemia is common at the time of anesthesia inductio

70 rdial contractility or induce hypotension if hypovolemia is corrected, and preliminary evidence sugge

71 Both HDTBR and hypovolemia led to a similar reduction in plasma volume.

72 n and perfusion index are further reduced by hypovolemia (lower body negative pressure, -60 mm Hg).

73 The etiologies of shock unrelated to hypovolemia must also be investigated.

74 ents, its effect on the indirect measures of hypovolemia needs to be clarified.

75 recognition of complicating physiology (eg, hypovolemia or cardiogenic shock), while invasive hemody

76 ption or maximal K+ secretion in response to hypovolemia or hyperkalemia, respectively.

77 ation from the scaling relation may indicate hypovolemia or hypervolemia and aid diagnosis.

78 ndogenous generation of Ang II during either hypovolemia or hypotension.

79 - areas previously shown to be activated by hypovolemia or peripheral angiotensin.

80 PEG; a colloid that produces non-hypotensive hypovolemia) or isoproterenol (hypotensive agent).

81 ossible underlying pathophysiologies include hypovolemia, partial dysautonomia, or a primary hyperadr

82 ce of a dry axilla supports the diagnosis of hypovolemia (positive likelihood ratio, 2.8; 95% CI, 1.4

83 by drinking hypertonic saline) and sustained hypovolemia (produced by subcutaneous injections of poly

84 Irreversible hypovolemia remains a major clinical problem.

85 identified as massive pulmonary embolism and hypovolemia, respectively.

86 Treatment with L-NAME during hypovolemia resulted in increased log low-frequency hear

87 After 50% hemorrhage followed by 1 hour of hypovolemia resuscitation with 35% of blood volume using

88 d finger perfusion index were reduced during hypovolemia/sham compared with normovolemia/sham.

89 activation in a setting of left ventricular hypovolemia stimulates ventricular afferents that trigge

90 analysis, the right ventricle was larger for hypovolemia than for primary arrhythmia (p < 0.001).

91 Among ICU patients with hypovolemia, the use of colloids vs crystalloids did not

92 efill (2C); for septic shock associated with hypovolemia, the use of crystalloids or albumin to deliv

93 tabolic acidosis is frequently attributed to hypovolemia, tissue hypoperfusion, and lactic acidosis.

94 nduced tissue hypoperfusion and suspicion of hypovolemia to achieve a minimum of 30 mL/kg of crystall

95 toire of putative clinical applications from hypovolemia to Alzheimer's disease.

96 ting to emergency departments with suspected hypovolemia, usually due to vomiting, diarrhea, or decre

97 rats with APX also was observed when marked hypovolemia was induced by s.c. administration of a hype

98 Central hypovolemia was induced with lower body negative pressur

99 Hypovolemia was maintained for 60 mins in test animals,

100 85 mL/kg) every 10 mins until 30% cumulative hypovolemia was reached.

101 Hypovolemia with reduced oxygen delivery and microvascul

102 ase in arterial pressure without evidence of hypovolemia, with a systolic pressure lower than 90 mm H