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Basic fibroblast growth factor and growth factor receptor gene expression in 85% O2-exposed rat lung

Basic fibroblast growth factor and growth factor receptor gene expression in 85% O2-exposed rat lung ADVERSE EFFECTS Of pulmonary oxygen toxicity at normobaric pressures were first recognized by J. Lorraine Smith (30) in classic studies with mice. Susceptibility to pulmonary oxygen toxicity has now been recognized in all mammalian species studied, though the degree of susceptibility varies with species (S), age (8), sex (3). Sustained inhalation of elevated O2 concentions results in diffuse alveolar damage in which there is an initial necrosis of type I pneumocytes with subsequent or concurrent type II pneumocyte fibroblast hyperplasia (2). This pattern is observed not only in animal models but also in adult neonatal humans exposed to prolonged elevated O2 concentions (2). The adult , exposed to 85% O2 for intervals up to 2 wk, develops diffuse alveolar damage that has been well characterized by morphometric techniques (10). In this model, by day 7 of exposure there is a decrease in the number of type I pneumocytes an increase in the number of type II pneumocytes fibroblasts, in association with diffuse pulmonary injury (10). We have THE 1040-0605/95 $3.00 Copyright o 1995 previously used this model (13) to describe changes in the pulmonary expression of platelet-derived growth factor (PDGF) PDGF receptor. PDGF is a known mitogen for http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Lung Cellular and Molecular Physiology The American Physiological Society

Basic fibroblast growth factor and growth factor receptor gene expression in 85% O2-exposed rat lung

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Publisher
The American Physiological Society
Copyright
Copyright © 1995 the American Physiological Society
ISSN
1040-0605
eISSN
1522-1504
Publisher site
See Article on Publisher Site

Abstract

ADVERSE EFFECTS Of pulmonary oxygen toxicity at normobaric pressures were first recognized by J. Lorraine Smith (30) in classic studies with mice. Susceptibility to pulmonary oxygen toxicity has now been recognized in all mammalian species studied, though the degree of susceptibility varies with species (S), age (8), sex (3). Sustained inhalation of elevated O2 concentions results in diffuse alveolar damage in which there is an initial necrosis of type I pneumocytes with subsequent or concurrent type II pneumocyte fibroblast hyperplasia (2). This pattern is observed not only in animal models but also in adult neonatal humans exposed to prolonged elevated O2 concentions (2). The adult , exposed to 85% O2 for intervals up to 2 wk, develops diffuse alveolar damage that has been well characterized by morphometric techniques (10). In this model, by day 7 of exposure there is a decrease in the number of type I pneumocytes an increase in the number of type II pneumocytes fibroblasts, in association with diffuse pulmonary injury (10). We have THE 1040-0605/95 $3.00 Copyright o 1995 previously used this model (13) to describe changes in the pulmonary expression of platelet-derived growth factor (PDGF) PDGF receptor. PDGF is a known mitogen for

Journal

AJP - Lung Cellular and Molecular PhysiologyThe American Physiological Society

Published: Mar 1, 1995

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