ライフサイエンスコーパス: lung edema

1 or mechanism that prevents the resolution of lung edema.

2 three-fold (p = 0.009), without significant lung edema.

3 , a worse LV remodeling index, and increased lung edema.

4 same large global strain, constantly produce lung edema.

5 s a unique therapeutic target in cardiogenic lung edema.

6 Na(+) channels (ENaCs) promotes cardiogenic lung edema.

7 e are also protected from ventilator-induced lung edema.

8 receptor inhibitor attenuated leptin-induced lung edema.

9 ccumulation, and vascular leakage leading to lung edema.

10 ation of neutrophils to the lungs as well as lung edema.

11 glutathione and increases endotoxin-mediated lung edema.

12 ity index are two promising early markers of lung edema.

13 jury is characterized histopathologically by lung edema and a neutrophil predominate leukocyte extrav

14 secretion may constitute a pathomechanism in lung edema and aimed to identify underlying molecular pa

15 currently being developed as a treatment for lung edema and has been shown to reduce extravascular lu

16 Hypoxia has been shown to cause lung edema and impair lung edema clearance.

17 CD47(-/-) neutrophils significantly reduced lung edema and neutrophil infiltration, thus demonstrati

18 ngiotensin-(1-7) blocked the protection from lung edema and protein leak, whereas A779 restored the i

19 gas exchange and lung compliance, prevented lung edema and pulmonary hypertension, and preserved ren

20 h should reflect the underlying lung injury (lung edema and recruitability).

21 neutrophil accumulation, the development of lung edema, and increased pulmonary production of IL-1be

22 pif(-/-) mice showed greater hypertrophy and lung edema as well as reduced survival in response to su

23 Acute epithelial lung injury, lung edema, bacteremia, and mortality were evaluated qua

24 Lung edema, bronchoalveolar lavage interleukin (IL)-6, a

25 nce (AFC) is necessary for the resolution of lung edema but is impaired in most patients with ARDS.

26 AQP1 facilitates hydrostatically driven lung edema but is not required for active near-isosmolar

27 th by altering vasoreactivity and increasing lung edema, but the acute effects of superoxide dismutas

28 ed transepithelial ion transport may promote lung edema by driving active alveolar fluid secretion.

29 g of gas exchange and histology suggest that lung edema can result from recurrent OAs.

30 s chamber dilation, ventricular dysfunction, lung edema, cardiac fibrosis, and apoptosis.

31 provide a novel treatment option to prevent lung edema caused by S. aureus alpha-toxin.

32 However, the effects of VALI on lung edema clearance and alveolar epithelial cells' Na,K

33 Dopamine (DA) increases lung edema clearance by stimulating vectorial Na+ flux a

34 Active Na+ transport and lung edema clearance decreased by approximately 44% in r

35 Lung edema clearance decreased by up to approximately 60

36 he importance of its role in contributing to lung edema clearance has been demonstrated.

37 However, the effects of this toxin on lung edema clearance have not been previously studied.

38 ine (TERB) and isoproterenol (ISO) increased lung edema clearance in control nonventilated rats (from

39 Lung edema clearance in control rats was 0.50 +/- 0.02 m

40 agonists increase active Na(+) transport and lung edema clearance in normal rat lungs by stimulating

41 to test whether DA (10(-)5 M) would increase lung edema clearance in rats exposed to 100% O2 for 64 h

42 ether beta-adrenergic agonists could restore lung edema clearance in rats ventilated with HVT (40 ml/

43 njury, decreases active sodium transport and lung edema clearance in rats.

44 DA increased lung edema clearance in room air breathing rats (from 0.

45 We studied lung edema clearance in the isolated-perfused rat lung m

46 t air spaces, the active Na(+) transport and lung edema clearance increased by approximately 53% as c

47 st that increased active Na(+) transport and lung edema clearance induced by aldosterone is probably

48 We previously reported that lung edema clearance was stimulated by dopamine (DA).

49 Paralleling the impairment in lung edema clearance we found a decrease in Na,K-ATPase

50 paminergic D(1) agonist fenoldopam increased lung edema clearance, but quinpirole (a specific dopamin

51 as been shown to cause lung edema and impair lung edema clearance.

52 terone may be used as a strategy to increase lung edema clearance.

53 alveolar epithelial cells and thus increases lung edema clearance.

54 n important role in active Na+ transport and lung edema clearance.

55 Lung edema, cytokines, and neutrophil counts were reduce

56 One of the lung edema dogs expired of acute heart failure in the se

57 f the PAR1-specific peptide TFLLRN increases lung edema during high-tidal-volume ventilation, and thi

58 k of ethanol ingestion significantly reduced lung edema during perfusion ex vivo.

59 reshold doses of TNF, which alone induced no lung edema, exacerbated S1P-induced edema and impaired s

60 Lung edema formation in this model was the result of mar

61 s in annealing AJs and thereby in preventing lung edema formation induced by endotoxin (LPS).

62 tion, which was associated with increases in lung edema formation, airway obstruction, and vascular e

63 stischemic lungs during reperfusion, reduces lung edema formation, and improves pulmonary function du

64 Data showed that lung edema formation, lung microvascular permeability, a

65 ion of proinflammatory cytokines and reduced lung edema formation.

66 However, rhAPC failed to prevent lung edema formation.

67 to the disruption of endothelial barrier and lung edema formation; however, the molecular mechanism o

68 Lung edema forms (possibly as an all-or-none response) d

69 n, as reflected by significant reductions in lung edema, hemorrhage, and thrombosis.

70 b (AZD5423) displayed a potent inhibition of lung edema in a rat model of allergic airway inflammatio

71 n-regulation increases survival and prevents lung edema in mice induced by bleomycin exposure-a lung

72 Hydrostatic lung edema in response to acute increases in pulmonary a

73 significantly upregulated and contribute to lung edema in ventilator-induced lung injury.

74 on of tight junctions in the lung and causes lung edema in vivo, which is prevented by genetic defici

75 ling cascade in the induction of PAF-induced lung edema, in that stimulation of ASM causes recruitmen

76 propionate) and prolonged the inhibition of lung edema, indicating potential for once-daily treatmen

77 MIP-2 in lung lavage, neutrophil influx, and lung edema measured at 48 h.

78 p47(phox-/-) mice, and an isolated perfused lung edema model that all point to a relationship betwee

79 distress syndrome, can be inactivated during lung edema, most likely by serum proteins.

80 from acute lung injury as evident by reduced lung edema, myeloperoxidase activity, histological lung

81 Similarly, LPS induced increases in lung edema, myeloperoxidase-concentrations, and pulmonar

82 PS-, acid-, and sepsis-induced ALI abolished lung edema, neutrophil infiltration, and tissue damage,

83 In PI3-Kgamma(-/-) mice, lung edema, neutrophil recruitment, nuclear translocatio

84 p < 0.05 vs. control), but did not decrease lung edema or improve CL.

85 protein concentration, BAL LDH activity, and lung edema (p < 0.05).

86 lung injury, as determined by development of lung edema, pulmonary neutrophil accumulation, histology

87 lung injury, as determined by development of lung edema, pulmonary neutrophil accumulation, lung IL-1

88 ion, high-tidal volume ventilation increased lung edema score and caused gas-exchange deterioration.

89 tients that have difficulty breathing due to lung edema, trauma, or general anesthesia.

90 ary gas exchange, whereas the development of lung edema was not affected.

91 e dehydrogenase (LDH) activity and increased lung edema was significantly associated with liver injur

92 activity (evaluated in the Sephadex model of lung edema) with reduced systemic toxicity (evaluated by