ライフサイエンスコーパス: VILI

1 d CO could serve to protect the lung against VILI.

2 t hypercapnic acidosis is protective against VILI in this model.

3 an increase in lung D2 is protective against VILI.

4 exchange, while an A2BAR agonist attenuated VILI.

5 A2BARs located on the lung tissue attenuated VILI-induced albumin leakage and pulmonary edema.

6 al a role for A2BAR signaling in attenuating VILI and implicate this receptor as a potential therapeu

7 mechanism(s) that recruit leukocytes during VILI have not been elucidated.

8 a suggest that NETs form in the lungs during VILI, contribute to the disease process, and thus may be

9 elevation of pulmonary cAMP levels following VILI, suggesting that A2BAR agonist treatment protects b

10 Expression profiling of lung tissues from VILI-challenged GADD45a(-/-) mice revealed strong dysreg

11 and whether the stress index could identify VILI better than compliance.

12 pliance and alveolar protein accumulation in VILI.

13 nhaled CO exerts antiinflammatory effects in VILI via the p38 mitogen-activated protein kinase pathwa

14 ic function of heme oxygenase-1 induction in VILI, we determined whether low concentration of inhaled

15 ociated with ventilator-induced lung injury (VILI) are unexplored.

16 ine model of ventilator-induced lung injury (VILI) correlated with injury and was reduced in hypercap

17 o understand ventilator-induced lung injury (VILI) during positive pressure ventilation, mechanisms o

18 olism during ventilator-induced lung injury (VILI) in mice.

19 ects against ventilator-induced lung injury (VILI) in vivo, we subjected 12 anesthetized, paralyzed r

20 Ventilator-induced lung injury (VILI) is a major cause of morbidity and mortality in int

21 Ventilator-induced lung injury (VILI) is characterized by inflammation.

22 The onset of ventilator-induced lung injury (VILI) is linked to a number of possible mechanisms.

23 r, MV causes ventilator-induced lung injury (VILI), a condition characterized by increased permeabili

24 use model of ventilator-induced lung injury (VILI), NETs were found in the lung microvasculature, and

25 n also cause ventilator-induced lung injury (VILI).

26 ity known as ventilator-induced lung injury (VILI).

27 ventilator-induced inflammatory lung injury (VILI).

28 d to prevent ventilator-induced lung injury (VILI).

29 nt models of ventilator-induced lung injury (VILI).

30 mation after ventilator-induced lung injury (VILI).

31 F attenuated ventilator-induced lung injury (VILI).

32 hat inhaled CO might be useful in minimizing VILI.

33 study, to ameliorate lung damage in a murine VILI model.

34 epithelial deformation in the development of VILI, we have developed an in vitro system in which chan

35 There are various forms of VILI, including volutrauma (i.e., injury caused by overd

36 context are in accord with the importance of VILI, and appear to show age-related susceptibility to V

37 to be a major component in the mechanism of VILI.

38 altered alveolar mechanics as a mechanism of VILI.

39 ADAM17 is an important proximal mediator of VILI; its inhibition is one mechanism of hypercapnic pro

40 G attenuates injury in this ex vivo model of VILI via mechanisms that prevent increases in permeabili

41 on was obtained in a two-hit murine model of VILI where pharmacological inhibition of ADAM17 reduced

42 ygenase-1 mRNA and protein in a rat model of VILI.

43 c microvascular leak of the present model of VILI.

44 investigated their role in a murine model of VILI.

45 h CXCR2 are important in the pathogeneses of VILI.

46 has been proposed to assess the presence of VILI.

47 The relevance of VILI in the pediatric intensive care unit population is

48 l Care Perspective analyzes the relevance of VILI to the pediatric population, and addresses why pedi

49 We hypothesized that VILI would cause systemic microvascular leak that is dep

50 n the tissue-protective effects of CO in the VILI model.

51 nts might be less susceptible than adults to VILI.

52 were found in hypothyroid WT mice exposed to VILI compared with euthyroid mice, indicating that the l

53 Mice exposed to VILI recapitulated the serum TH findings of acute illnes

54 proposed ventilator settings expose lungs to VILI during EVLP and whether the stress index could iden

55 rently proposed for EVLP may expose lungs to VILI.

56 Here, we profiled the response to VILI in mice with genetic deletions of each of the 4 ade

57 ne and cytokine profiles seen in response to VILI, demonstrating a role for T(3) in the treatment of

58 role of caveolin-1 in lung susceptibility to VILI in mice.

59 2KO mice exhibited greater susceptibility to VILI than WT mice, as evidenced by poorer alveoli integr

60 appear to show age-related susceptibility to VILI, although a conclusive link between use of large Vt

61 Caveolin-1 null mice are more susceptible to VILI.

62 profoundly susceptible to high tidal volume VILI, with increases in microvascular permeability and b

63 the morbidity and mortality associated with VILI.