| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Original Articles |
The pathogenic mechanisms of lipopolysaccharide (LPS)-induced lung injury have not been classified. This study examined the physiological changes after endotoxin inhalation and related those to features of pulmonary inflammation in mice. Pulmonary mechanics, histopathology, and bronchoalveolar lavage fluid (BALF) from BALB/c mice were analysed at different occasions (3, 24, 48 and 72 h) after inhalation of saline or LPS from Escherichia coli (0.3 (L0.3) or 10 mg x mL(-1) (L10)). Mice were sedated, anaesthetized, and ventilated. After chest wall resection static (Est) and dynamic (Edyn) elastances, deltaE (Edyn-Est), resistive (deltaP1) and viscoelastic/inhomogeneous pressures (deltaP2), and deltaP1+deltaP2 (deltaPtot) were obtained by end-inflation occlusion method. Lungs were prepared for histopathology. In parallel groups, tumour necrosis factor (TNF)-alpha, neutrophils, and protein were evaluated in the BALF. L0.3 and L10 showed a time-dependent production of TNF-alpha preceding a massive neutrophil infiltration. In L10 BALF there was an increase in protein level at 24 and 48 h. Est and Edyn increased early in L0.3 (65%, 63%) and L10 (41%, 51%). In L10 deltaE, deltaP2, and deltaPtot showed a gradual rise. At 72 h all groups were similar. L0.3 showed an early increase in cellularity, which returned to normal at 72 h. L10 presented the same pattern with the cell count remaining elevated until 72 h. In conclusion, lipopolysaccharide inhalation led to elastic and viscoelastic pulmonary changes together with tumour necrosis factor-alpha production and neutrophil infiltration in mouse lung.
This article has been cited by other articles:
|
|
 |
|
  J. Haller, D. Hyde, N. Deliolanis, R. de Kleine, M. Niedre, and V. Ntziachristos Visualization of pulmonary inflammation using noninvasive fluorescence molecular imaging J Appl Physiol, March 1, 2008; 104(3): 795 - 802. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. B. Santos, L. K. S. Nagato, N. M. Boechem, E. M. Negri, A. Guimaraes, V. L. Capelozzi, D. S. Faffe, W. A. Zin, and P. R. M. Rocco Time course of lung parenchyma remodeling in pulmonary and extrapulmonary acute lung injury J Appl Physiol, January 1, 2006; 100(1): 98 - 106. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Ramphal, V. Balloy, M. Huerre, M. Si-Tahar, and M. Chignard TLRs 2 and 4 Are Not Involved in Hypersusceptibility to Acute Pseudomonas aeruginosa Lung Infections J. Immunol., September 15, 2005; 175(6): 3927 - 3934. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. D. Puri, T. A. Doggett, C.-Y. Huang, J. Douangpanya, J. S. Hayflick, M. Turner, J. Penninger, and T. G. Diacovo The role of endothelial PI3K{gamma} activity in neutrophil trafficking Blood, July 1, 2005; 106(1): 150 - 157. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Allen and J. H. T. Bates Dynamic mechanical consequences of deep inflation in mice depend on type and degree of lung injury J Appl Physiol, January 1, 2004; 96(1): 293 - 300. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P.R.M. Rocco, D.P. Momesso, R.C. Figueira, H.C. Ferreira, R.A. Cadete, A. Legora-Machado, V.L.G. Koatz, L.M. Lima, E.J. Barreiro, and W.A. Zin Therapeutic potential of a new phosphodiesterase inhibitor in acute lung injury Eur. Respir. J., July 1, 2003; 22(1): 20 - 27. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Beckmann, B. Tigani, R. Sugar, A. D. Jackson, G. Jones, L. Mazzoni, and J. R. Fozard Noninvasive detection of endotoxin-induced mucus hypersecretion in rat lung by MRI Am J Physiol Lung Cell Mol Physiol, July 1, 2002; 283(1): L22 - L30. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
