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Articles in PresS, published online ahead of print October 11, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00158.2002
Submitted on May 20, 2002
Accepted on October 9, 2002
1 Institute of Physiology, University of Zurich, Zurich, Zurich, Switzerland; Institute of Anesthesiology, University of Zurich, Zurich, Zurich, Switzerland
2 Institute of Physiology, University of Zurich, Zurich, Zurich, Switzerland
3 Institute of Anatomy, University of Zurich, Zurich, Zurich, Switzerland
4 Paul Scherrer Institute, Villigen, Aargau, Switzerland
5 Institute of Anesthesiology, University of Zurich, Zurich, Zurich, Switzerland
6 Department of Surgery, University of Zurich, Zurich, Zurich, Switzerland
7 Institute of Anesthesiology, University of Zurich, Zurich, Zurich, Switzerland; Institute of Physiology, University of Zurich, Zurich, Zurich, Switzerland
* To whom correspondence should be addressed. E-mail: bbeck{at}physiol.unizh.ch.
Molecular mechanisms of the inflammatory reaction in hypoxia-induced lung injury are not well defined. Therefore, effects of alveolar hypoxia were studied in rat lungs, exposing rats to 10% oxygen over periods of 1, 2, 4, 6 and 8 hours. An increase in the number of macrophages in bronchoalveolar lavage fluid of hypoxic animals was shown between 1 and 8 hours. Extravasation of albumin was enhanced already after 1 hour, and remained increased throughout the study period. NF-
B-binding activity as well as mRNA for TNF-
, MIP-1ß and MCP-1 were increased within the first 2 hours of exposure to hypoxia. HIF-1 and ICAM-1 mRNA were up-regulated between 1 and 6 hours. Elimination of alveolar macrophages by intratracheal application of liposome-encapsulated clodronate lead to a decreased expression of NF-B binding activity, HIF-1, TNF-, ICAM-1 and MIP-1ß. In summary, alveolar hypoxia induced macrophage recruitment, an increase in albumin leakage, and enhanced expression of inflammatory mediators, which were mainly macrophage-dependent. Alveolar macrophages appear to have a prominent role in the inflammatory response in hypoxia-induced lung injury and the related up-regulation of inflammmatory mediators.
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