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1 by reducing lung inflammation and enhancing alveolar fluid clearance.
2 nary edema by up-regulating sodium-dependent alveolar fluid clearance.
3 eolar epithelial fluid transport measured as alveolar fluid clearance.
4 ndothelial barrier permeability and restored alveolar fluid clearance.
5 mechanisms may contribute to the decrease in alveolar fluid clearance.
6 bited both basal and beta agonist-stimulated alveolar fluid clearance.
7 is, neutrophil activation and clearance, and alveolar fluid clearance.
8 elial permeability to protein, and decreased alveolar fluid clearance.
9 ed elevated lung inflammation and attenuated alveolar fluid clearance.
10 a level comparable to maximal cAMP-dependent alveolar fluid clearance.
11 samples were associated with slower rates of alveolar fluid clearance.
12 genous catecholamines did not correlate with alveolar fluid clearance.
13 in and an approximately 50% reduction in net alveolar fluid clearance.
14 id instillation led to a 50% decrease in net alveolar fluid clearance.
15 ANTU-induced edema formation by potentiating alveolar fluid clearance.
16 mild pulmonary oedema (24/29 [83%]), intact alveolar fluid clearance (17/23 [74%]), and normal or mi
17 ith serial samples, there was a high rate of alveolar fluid clearance (19 +/- 9%/h, mean +/- SD).
18 lar epithelial dysfunction, as determined by alveolar fluid clearance (AFC) and intra-alveolar levels
20 h acute lung injury (ALI) who retain maximal alveolar fluid clearance (AFC) have better clinical outc
22 of the NO donor, DETANONOate, would decrease alveolar fluid clearance (AFC) in the rabbit in vivo.
23 nfected with M. pulmonis for measurements of alveolar fluid clearance (AFC) in vivo and isolation of
24 reactive byproducts inhibit Na(+)-dependent alveolar fluid clearance (AFC) in vivo and the activity
26 Whether these receptors are essential for alveolar fluid clearance (AFC) or if other mechanisms ar
29 A(2a)R- or A(3)R-specific agonists increased alveolar fluid clearance (AFC), whereas physiologic conc
31 aspiration-induced lung injury by increasing alveolar fluid clearance and decreasing endothelial perm
32 hese data suggest that claudin-4 may promote alveolar fluid clearance and demonstrate that the amount
33 subunit plasmid showed a twofold increase in alveolar fluid clearance and Na(+),K(+)-ATPase activity
34 ce to lung injury, db/db mice had diminished alveolar fluid clearance and reduced Na,K-ATPase functio
36 nce, fibrinogenesis, inflammatory cytokines, alveolar fluid clearance, and endothelial injury and act
37 panied by a 2.4-fold increase in the rate of alveolar fluid clearance at 4 hrs in the salmeterol-trea
39 with control, LTD4 (1 x 10(-11) M) increased alveolar fluid clearance by 41% (p < 0.001) in isolated,
40 in BALB/c mice increased amiloride-sensitive alveolar fluid clearance by approximately 30%, consisten
41 ung and restored the normal up-regulation of alveolar fluid clearance by catecholamines after prolong
42 e lung prevented the normal up-regulation of alveolar fluid clearance by catecholamines following hem
49 edema and acute lung injury, we measured net alveolar fluid clearance in 79 patients with acute lung
50 ring the beta- adrenergic agonist-stimulated alveolar fluid clearance in acute lung injury, an effect
54 in contrast to hydrostatic pulmonary edema, alveolar fluid clearance in patients with acute lung inj
57 red in the majority of patients, and maximal alveolar fluid clearance is associated with better clini
63 nction protein claudin-4 are associated with alveolar fluid clearance or clinical measures of lung fu
67 human lungs, mesenchymal stem cells restored alveolar fluid clearance, reduced inflammation, and exer
68 ing demonstrated a positive correlation with alveolar fluid clearance (Spearman rank correlation [r(s
69 Concomitantly, we observed a reversal of alveolar fluid clearance, suggesting that reversed trans
70 ts with acute lung injury (ALI) have reduced alveolar fluid clearance that has been associated with h
71 , and isoproterenol 10(-6) M each stimulated alveolar fluid clearance to a level comparable to maxima
72 -grade human mesenchymal stem cells restored alveolar fluid clearance to a normal level, decreased in
74 th hydrostatic pulmonary edema, in whom mean alveolar fluid clearance was 13%/h; only 25% had impaire
87 eduction of Na,K-ATPase expression decreases alveolar fluid clearance, which in turn leads to pulmona
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