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1 y observed in patients with ARDS by creating ventilator-induced lung injury.
2 r vessels may be important in the genesis of ventilator-induced lung injury.
3 severe and more homogeneous distribution of ventilator-induced lung injury.
4 ated whether fat feeding protected mice from ventilator-induced lung injury.
5 stress and strain are major determinants of ventilator-induced lung injury.
6 rve as potential biomarkers and mediators of ventilator-induced lung injury.
7 associated with disease-specific features of ventilator-induced lung injury.
8 nsequences of mechanical ventilation such as ventilator-induced lung injury.
9 tory process accompanying early experimental ventilator-induced lung injury.
10 ate acute lung injury by causing a secondary ventilator-induced lung injury.
11 ked OxPAPC protection from interleukin-6 and ventilator-induced lung injury.
12 and minimize/abolish the harmful effects of ventilator-induced lung injury.
13 d alveolar pressure that could contribute to ventilator-induced lung injury.
14 nimal and endothelial cell culture models of ventilator-induced lung injury.
15 reviously verified two-hit model of in vitro ventilator-induced lung injury.
16 ch plays a major role in the pathogenesis of ventilator-induced lung injury.
17 r function, and inflammation associated with ventilator-induced lung injury.
18 in lung mechanics and in the pathogenesis of ventilator-induced lung injury.
19 sion blocked OxPAPC-mediated protection from ventilator-induced lung injury.
20 odels of bleomycin-induced lung fibrosis and ventilator-induced lung injury.
21 repair by confocal microscopy in a model of ventilator-induced lung injury.
22 LT(1) receptor antagonist, largely prevented ventilator-induced lung injury.
23 s and accumulated in lungs from animals with ventilator-induced lung injury.
24 aluronan synthase 3, and was associated with ventilator-induced lung injury.
25 upregulated and contribute to lung edema in ventilator-induced lung injury.
26 me and driving pressure, key determinants of ventilator-induced lung injury.
27 expression and activity in a mouse model of ventilator-induced lung injury.
28 plays a role in the inflammatory response of ventilator-induced lung injury.
29 lung injury in a large tidal volume model of ventilator-induced lung injury.
30 and NO may contribute to the development of ventilator-induced lung injury.
31 mmatory mediator release, suggesting reduced ventilator-induced lung injury.
32 ncrease CO2 removal and therefore may reduce ventilator-induced lung injury.
33 n, multiple system organ failure, and severe ventilator-induced lung injury.
34 alveolar instability can independently cause ventilator-induced lung injury.
35 he effects of increasing inspiratory time on ventilator-induced lung injury.
36 the oleic acid injury (0.67 of baseline) or ventilator-induced lung injury (0.79 of baseline) models
37 r the magnitude of blood flow contributes to ventilator-induced lung injury, 14 sets of isolated rabb
40 has led to advances in the understanding of ventilator-induced lung injury and in optimizing the sup
41 led to advances both in our understanding of ventilator-induced lung injury and in optimizing the sup
42 highlights strategies directed at minimizing ventilator-induced lung injury and other new adjunctive
43 observed in vivo in the mouse 2-hit model of ventilator-induced lung injury and were linked to MT sta
45 ils into the lung is an important feature of ventilator-induced lung injury associated with pneumonia
46 EP levels may improve oxygenation and reduce ventilator-induced lung injury but may also cause circul
48 Mechanical ventilator strategies that limit ventilator-induced lung injury by avoiding hyperventilat
49 P permits unstable alveoli and may result in ventilator-induced lung injury despite improved oxygenat
50 gas exchange and afford lung protection from ventilator-induced lung injury during high-pressure mech
53 stigated the impact of two distinct forms of ventilator-induced lung injury, i.e., volutrauma and ate
54 imize or even abolish the harmful effects of ventilator-induced lung injury if used as an alternative
56 mption of a high-fat diet protects mice from ventilator-induced lung injury in a manner independent o
58 y be a promising strategy for alleviation of ventilator-induced lung injury in critically ill patient
61 strated a markedly dependent distribution of ventilator-induced lung injury in oleic acid-injured sup
62 Fat-fed mice showed clear attenuation of ventilator-induced lung injury in terms of respiratory m
63 eatly from our previous sheep model of acute ventilator-induced lung injury in which sheep were venti
65 riggered mechanism in the protection against ventilator-induced lung injury involves cyclooxygenase 2
69 eir relative contribution to inflammation in ventilator-induced lung injury is not well established.
70 It has been postulated that the mechanism of ventilator-induced lung injury is the result of heteroge
71 igned to 4 hours of ventilation of the left (ventilator-induced lung injury) lung with tidal volume o
75 of hydrogen sulfide were analyzed in a mouse ventilator-induced lung injury model in vivo as well as
76 RM caused a lasting increase of PaO2 in the ventilator-induced lung injury model, but in oleic acid
79 cute lung injury: oleic acid injury (n = 4); ventilator-induced lung injury (n = 4); and pneumonia (n
80 y develop lung injury that is similar to the ventilator-induced lung injury observed in mechanically
81 nd poorly aerated regions was also higher in ventilator-induced lung injury piglets compared with con
82 oro-2-deoxy-D-glucose uptakes were higher in ventilator-induced lung injury piglets compared with con
83 e in children have been targeted at reducing ventilator-induced lung injury, providing treatment adju
85 (ALI) associated with sepsis and iatrogenic ventilator-induced lung injury resulting from mechanical
89 n, is associated with known risk factors for ventilator-induced lung injury such as ventilation with
90 use circulatory depression and contribute to ventilator-induced lung injury through alveolar overdist
91 higher [F]fluorodeoxyglucose uptake rate in ventilator-induced lung injury versus control lung (0.01
92 ts, but the systemic effects associated with ventilator-induced lung injury (VILI) are unexplored.
93 p44/42 MAPK activation in a murine model of ventilator-induced lung injury (VILI) correlated with in
96 hether hypercapnic acidosis protects against ventilator-induced lung injury (VILI) in vivo, we subjec
101 ophil- and platelet-dependent mouse model of ventilator-induced lung injury (VILI), NETs were found i
110 of ventilator care and decrease the risk of ventilator-induced lung injury, we designed and tested a
111 ts alveolar barrier disruption in a model of ventilator-induced lung injury, we examined alveolar bar
112 ONALE: In the original 1974 in vivo study of ventilator-induced lung injury, Webb and Tierney reporte
113 nfirm that unstable alveoli are subjected to ventilator-induced lung injury whereas stable alveoli ar
114 hanically ventilated patients is the risk of ventilator-induced lung injury, which is partially preve
116 nfirm that unstable alveoli are subjected to ventilator-induced lung injury while stable alveoli are
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