| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Department of Human Physiology, School of Medicine, Flinders University of South Australia, and Departments of 2 Critical Care Medicine and 3 Anatomical Pathology, Flinders Medical Centre, Bedford Park, South Australia 5042, Australia
Although acute lung injury (ALI) is associated with inflammation and surfactant dysfunction, the precise sequence of these changes remains poorly described. We used oleic acid to study the pathogenesis of ALI in spontaneously breathing anesthetized rats. We found that lung pathology can occur far more rapidly than previously appreciated. Lung neutrophils were increased approximately threefold within 5 min, and surfactant composition was dramatically altered within 15 min. Alveolar cholesterol increased by ~200%, and even though disaturated phospholipids increased by ~30% over 4 h, the disaturated phospholipid-to-total phospholipid ratio fell. Although the alveolocapillary barrier was profoundly disrupted after just 15 min, with marked elevations in lung fluid (99mTc-labeled diethylenetriamine pentaacetic acid) and 125I-labeled albumin flux, the lung rapidly began to regain its sieving properties. Despite the restoration in lung permeability, the animals remained hypoxic even though minute ventilation was increased approximately twofold and static compliance progressively deteriorated. This study highlights that ALI can set in motion a sequence of events continuing the respiratory failure irrespective of the alveolar surfactant pool size and the status of the alveolocapillary barrier.
static lung compliance; alveolocapillary permeability; respiratory pathophysiology; lysophosphatidylcholine; alveolar protein
This article has been cited by other articles:
|
|
 |
|
  S. Lin, J. Walker, L. Xu, D. Gozal, and J. Yu Respiratory: Behaviours of pulmonary sensory receptors during development of acute lung injury in the rabbit Exp Physiol, July 1, 2007; 92(4): 749 - 755. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Rodrigo, S. Trujillo, and C. Bosco Biochemical and Ultrastructural Lung Damage Induced by Rhabdomyolysis in the Rat Experimental Biology and Medicine, September 1, 2006; 231(8): 1430 - 1438. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Ulrich, M. Stern, M. E. Goddard, J. Williams, J. Zhu, A. Dewar, H. A. Painter, P. K. Jeffery, D. R. Gill, S. C. Hyde, et al. Keratinocyte growth factor therapy in murine oleic acid-induced acute lung injury Am J Physiol Lung Cell Mol Physiol, June 1, 2005; 288(6): L1179 - L1192. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Matalon and H.-L. Ji Oleic Acid Damages Ion Transport and Promotes Alveolar Edema: The Dark Side of Healthy Living Am. J. Respir. Crit. Care Med., March 1, 2005; 171(5): 424 - 425. [Full Text] [PDF]
|
|
|
|
|
|
M. Christofidou-Solomidou, A. Scherpereel, R. Wiewrodt, K. Ng, T. Sweitzer, E. Arguiri, V. Shuvaev, C. C. Solomides, S. M. Albelda, and V. R. Muzykantov PECAM-directed delivery of catalase to endothelium protects against pulmonary vascular oxidative stress Am J Physiol Lung Cell Mol Physiol, August 1, 2003; 285(2): L283 - L292. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. G. De Pasquale, A. D. Bersten, I. R. Doyle, P. E. Aylward, and L. F. Arnolda Infarct-induced chronic heart failure increases bidirectional protein movement across the alveolocapillary barrier Am J Physiol Heart Circ Physiol, June 1, 2003; 284(6): H2136 - H2145. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. G. Davidson, A. D. Bersten, H. A. Barr, K. D. Dowling, T. E. Nicholas, and I. R. Doyle Endotoxin Induces Respiratory Failure and Increases Surfactant Turnover and Respiration Independent of Alveolocapillary Injury in Rats Am. J. Respir. Crit. Care Med., June 1, 2002; 165(11): 1516 - 1525. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
