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Expression of Endothelial Nitric Oxide Synthase, Inducible Nitric Oxide Synthase, and Endothelin-1 in Lungs of Subjects Who Died With ARDS*

K. H. Albertine, PhD; Z. M. Wang; J. R. Michael
Author and Funding Information

*From the University of Utah, Salt Lake City, UT. Supported by NIH SCOR grant P50 HL50153.

Correspondence to: K. H. Albertine, PhD, University of Utah School of Medicine, 50 N Medical Dr, Room 2A129, Salt Lake City, UT 84132-1001



Chest. 1999;116(suppl_1):101S-102S. doi:10.1378/chest.116.suppl_1.101S
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Extract

Persistent pulmonary inflammation and pulmonary hypertension are characteristics of subjects with ARDS. Among the contributing factors to the pathophysiology of ARDS, two enzymes and a peptide are of particular interest: endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), and endothelin-1 (ET-1). It is unclear which cells in the lungs of ARDS subjects express these mediators, or how their pattern of expression compares to expression in the lungs of subjects who have nonpulmonary disease. To this end, we performed quantitative immunohistochemistry for eNOS, iNOS, and ET-1 in lung tissue obtained from six subjects who died with ARDS and six subjects who died without ARDS. We used monoclonal antibodies, antigen-retrieval immunoperoxidase methods (with relevant controls), and light microscopic densitometry to compare the distribution of each mediator between the two groups. For light microscopic densitometry, five random fields each were drawn across pulmonary arterial endothelial and smooth muscle cells, airway epithelial cells, and alveolar macrophages. Nuclei were excluded. The image analysis system automatically determined the brown immunostain density. This procedure was repeated for at least 10 vessels, airways, and alveolar macrophages per subject.


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