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A new model of progressive pulmonary fibrosis in rats.

Authors
Last-JA; Gelzleichter-TR; Pinkerton-KE; Walker-RM; Witschi-H
Source
Am Rev Respir Dis 1993 Aug; 148(2):487-494
NIOSHTIC No.
20033130
Abstract
Sprague-Dawley rats were exposed for 6 h daily to 0.8 ppm of ozone and 14.4 ppm of nitrogen dioxide. Approximately 7 to 10 wk after the initiation of exposure, animals began to demonstrate respiratory insufficiency and severe weight loss. About half of the rats died between Days 55 and 78 of exposure; no overt ill effects were observed in animals exposed to filtered air, to ozone alone, or to nitrogen dioxide. Biochemical findings in animals exposed to ozone and nitrogen dioxide included increased lung content of DNA, protein, collagen, and elastin, which was about 300% higher than the control values. The collagen-specific crosslink hydroxy-pyridinium, a biomarker for mature collagen in the lung, was decreased by about 40%. These results are consistent with extensive breakdown and remodeling of the lung parenchyma and its associated vasculature. Histopathologic evaluation showed severe fibrosis, alveolar collapse, honeycombing, macrophage and mast cell accumulation, vascular smooth muscle hypertrophy, and other indications of severe progressive interstitial pulmonary fibrosis and end-stage lung disease. This unique animal model of progressive pulmonary fibrosis resembles the final stages of human idiopathic pulmonary fibrosis and should facilitate studying underlying mechanisms and potential therapy of progressive pulmonary fibrosis.
Keywords
Animal-studies; Animals; Exposure-assessment; Exposure-levels; Exposure-limits; Respiratory-function-tests; Respiratory-hypersensitivity; Respiratory-irritants; Respiratory-rate; Respiratory-system-disorders; Chemical-hypersensitivity; Chemical-indicators; Chemical-reactions; Chemical-structure; Chemical-synthesis; Mortality-data; Mortality-rates; Mortality-surveys; Histopathology; Analytical-Method; Muscle-function; Muscle-necrosis; Muscle-physiology; Muscle-tissue; Muscles; Pulmonary-clearance; Pulmonary-congestion; Pulmonary-disorders; Pulmonary-function; Pulmonary-function-tests; Pulmonary-system; Pulmonary-system-disorders; Fibrogenesis; Fibrogenicity; Fibrosis
Contact
J. A. Last, Department of Internal Medicine, School of Medicine, University of California, Davis 95616-8542
CODEN
ARDSBL
Publication Date
19930801
Document Type
Journal Article
Funding Amount
1055222
Funding Type
Cooperative Agreement
Fiscal Year
1993
NTIS Accession No.
NTIS Price
Identifying No.
Cooperative-Agreement-Number-U07-CCU-906162
Issue of Publication
2
ISSN
0003-0805
Source Name
American Review of Respiratory Disease
State
CA
Performing Organization
University of California - Davis
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