Warning: fopen(/home/virtual/jptm/journal/upload/ip_log/ip_log_2022-11.txt): failed to open stream: Permission denied in /home/virtual/lib/view_data.php on line 83 Warning: fwrite() expects parameter 1 to be resource, boolean given in /home/virtual/lib/view_data.php on line 84 Journal of Pathology and Translational Medicine
Skip Navigation
Skip to contents

JPTM : Journal of Pathology and Translational Medicine

OPEN ACCESS
SEARCH
Search

Articles

Page Path
HOME > J Pathol Transl Med > Volume 21(3); 1987 > Article
Original Article Mechanisms of Experimental Pulmonary Fibrosis Following Paraquat Toxicity.
Sang Sook Lee, Chai Hong Chung, Tae Jung Sohn
Journal of Pathology and Translational Medicine 1987;21(3):111-137
DOI: https://doi.org/
  • 1,240 Views
  • 17 Download
  • 0 Crossref
  • 0 Scopus
1Department of Pathology, Keimyung University School of Medicine, Taegu, Korea.
2Department of Pathology, Kyungpook National University School of Medicine, Taegu, Korea.

This study was carried out to investigate the intricate mechanisms of intraalveolar fibrosis, leading to the alveolar structural remodeling, of rat lungs treated with paraquat. Sixty-three male Sprague-Dawley rats, maintained on a stock diet, weighing 200.0 gm, average, were divided into 4 experimental groups. Group 1. Control group (10 rats). Intraperitoneal injections of 2-4 ml normal saline only. Group 2(13 rats). 10, 20, 25, 30 and 40 mg per kg of body weight was administered intraperitoneally. Animals were sacificed 5 hours. 1 and 3 days after paraquat treatment. Group 3(16 rats). 20, 25, 30 and 40 mg per kg of body weight was administered to the animal, and animals died 2-5 days after paraquat administration. Group 4(24 rats). The same amount of paraquat was administered to the animal as in the group 2. Animals were sacrificed 1, 2, 6, 8 and 10 weeks after paraquat treatment. Sacrificed animal lung was examined by gross, light-microscopic, immunohistochemical, ultrastructural observation, along with cellular and chemical analyses of bronchoalveolar lavage fluid. The results were as follows: Grossly, 6 rats of chronic stage (1-10 weeks survival) developed multiple wedge-shaped scars on both lungs. These scars were situated mainly along the bronchial trees, blood vessels and subpleural regions. Light microscopically, the salient features found of the chronic stage lungs were intraalveolar fibrosis. Intraluminal buds or polypoid masses projecting into the alveolar lumen and ducts. Elsewhere, loose connective tissue masses were found to fuse together to alveolar wall, obliterating the alveolar spaces with resultant severe alveolar structural remodeling. Immunohistochemically, fibronectin was found in the center of intraalveolar buds and polypoid mass, projecting into the alveolar lumen, and in the adjacent proliferating alveolar macrophages. An attempt to measure the amount of fibronectin in the bronchoalveolar lavage fluid failed. Electron microscopically, the chronic stage lung revealed marked proliferation of both alveolar macrophages and fibroblasts in the alveolar spaces, the latter containing actin-like microfilaments and collagen fibers arranged in bundles and spirals. In areas, myofibroblasts and smooth muscle cells also present. Cellular analysis of the bronchoalveolar lavage fluid in chronic stage lungs revealed no significant findings. It can be concluded, therefore: That intraalveolar fibrosis of the paraquat-treated lungs of the rat is probably mediated by intraalveolar migrations of the interstitial cells, the main task force being the connective tissue cells, passing through the defects created in the epithelial lining surface to its basement membrane, which were inflicted upon the alveolar wall by paraquat toxicity. Fibronectin, released by activated alveolar macrophages, may be responsible for the migrations of fibroblasts and myofibroblasts into the alveolar spaces to form the intraalveolar fibrosis with subsequent alveolar structural remodeling,

Related articles

JPTM : Journal of Pathology and Translational Medicine