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1 epletion model of ARDS was created by saline lung lavage.
2 ss syndrome was induced by repetitive saline lung lavage.
3 and is also available in saliva, plasma, and lung lavage.
4 -6) reacted with a double band of 290 kDa in lung lavage.
5 Acute lung injury was induced by saline lung lavage.
6 ased concentrations of the chemokine CCL2 in lung lavage.
7 e lung injury was induced by repeated saline lung lavage.
8 w) settings in five piglets before and after lung lavage.
9 n at the same mean airway pressure as before lung lavage.
10 s syndrome model was established by repeated lung lavages.
11 Lung injury was created by repeated saline lung lavages.
16 lary endothelium and cytokine levels in both lung lavage and supernatants from cultured lymph node ly
20 antibodies specific for B. melitensis LPS in lung lavages and specific IgG and IgA antibody-secreting
22 IgA LPS-specific antibodies were detected in lung lavages, and specific antibody-secreting cells were
23 lude that dilute surfactants administered by lung lavage are effective in reversing pulmonary dysfunc
25 tocopherol were inhibitory and reversible in lung lavage but, importantly, were proinflammatory in lu
26 N-gamma-producing CD4+ and CD8+ cells in the lung lavages but no change in the number of IL-4-produci
28 onchoalveolar lymphocytes and the ability of lung lavage cells to produce proinflammatory cytokines w
30 reased lung neutrophil accumulation, but not lung lavage cytokine-induced neutrophil chemoattractant
31 s in lung lavage neutrophil accumulation and lung lavage cytokine-induced neutrophil chemoattractant
32 pite the fact that 22% had CMV isolated from lung lavage fluid and 32% had CMV isolated from blood.
34 rleukin-8 (IL-8), and GRO were detectable in lung lavage fluid at 4 h and declined by 24 h in animals
35 sponse in the lung as determined by assay of lung lavage fluid by enzyme-linked immunosorbent assay a
37 pies per microliter and influenza A virus in lung lavage fluid containing 2.08 x 10(6) viral copies p
39 CSF protein levels were observed in sera and lung lavage fluid from superinfected animals, suggesting
40 niae organisms are frequently present in the lung lavage fluid from this cohort of predominantly asth
44 Reduction in inflammatory cytokine levels in lung lavage fluid samples correlated with the clinical o
46 ats given IL-1 intratracheally had increased lung lavage fluid tumor necrosis factor (TNF) levels, an
48 vated tocopherols on tissue inflammation and lung lavage fluid were reversible in a second phase of A
49 hione levels in the plasma, lung tissue, and lung lavage fluid, and increased (P < 0.05) oxidized glu
51 ens, such as turbinate tissue homogenate and lung lavage fluid, as well as antemortem samples, such a
52 can assay GSH in whole blood, plasma, serum, lung lavage fluid, cerebrospinal fluid, urine, tissues a
54 cytokines interleukin-5 (IL-5) and IL-13 in lung lavage fluid, decreased regulatory T cell-associate
55 tal protein and proinflammatory cytokines in lung lavage fluid, enhanced LPS-mediated signaling in lu
68 e correlated the quantity of leukotrienes in lung lavage fluids of infected mice with respiratory rat
70 inin peptides were identical to sequences in lung (lavage) gp-340, a member of the scavenger receptor
71 lar lavage (BAL) in human subjects and whole-lung lavage in mice following a single inhalation exposu
73 led very high percentages of Th17.1 cells in lung lavage in sarcoidosis compared with controls in two
75 nificantly more monocytes and neutrophils in lung lavage, increased CD4+/CD8+ T-lymphocyte ratio, and
76 curs following the use of open suctioning in lung lavage injured sheep and whether the baseline PaCO2
85 Fbp intravenously had the same elevations in lung lavage neutrophil accumulation and lung lavage cyto
87 xhibited a twofold increase in the number of lung lavage neutrophil level whereas NGFR knockout mice
88 activation, concentration of KC and MIP-2 in lung lavage, neutrophil influx, and lung edema measured
91 of all classes of leukocytes recovered from lung lavages of infected neonates and adults were simila
92 ng IFNgamma than those producing IL-4 in the lung lavages of mice given either syngeneic or allogenei
95 sures of lung injury including gas exchange, lung lavage protein and lactate dehydrogenase (LDH), lun
98 tent, lung leak index, lung weight gain, and lung lavage protein concentrations were increased in rat
99 lymphocyte precursor frequency, NO levels in lung lavage, rates of virus clearance, and anti-RSV Ab t
100 at each level of mean airway pressure after lung lavage, respiratory system compliance and functiona
102 (inactive) forms of IL-33 can be detected in lung lavage samples from mice challenged with Alternaria
109 on eight septic rats and on seven controls; lung lavage was performed on three septic rats and three
111 y of the patient's symptoms, bilateral whole-lung lavage was undertaken, leading to symptomatic impro
113 nts with PAP who underwent therapeutic whole-lung lavage were compared with those of 10 healthy volun
114 Hsp70 levels in lung tissue and in cell-free lung lavage were increased compared with mice exposed to
115 nterferon, or tumor necrosis factor alpha in lung lavages were found between CCL3(+/+) and CCL3(-/-)
117 g injury was induced in 23 sheep by repeated lung lavage with warmed saline until the PaO2/FIO2 ratio
118 stress syndrome was induced combining saline lung lavages with injurious mechanical ventilation.
119 were determined in noninjured (n = 9) and in lungs lavaged with saline (n = 8) at quasi-static (low f
120 s (4-4.5 mg phospholipid/ml) administered by lung lavage would be equally effective in reversing pulm
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