Abstract:
:Previous studies have demonstrated a role for the beta-adrenergic system in the maturation of the fetal alveolar epithelium. Chronic blockade of beta-adrenergic binding sites has been shown to adversely effect physiologic and biochemical indices of fetal lung maturation. In the present study timed-pregnant female Sprague-Dawley rats were treated with a continuous 0.5 mg/hr dose of propranolol HCl, or saline, via an osmotic pump. The treatment periods were days 18-21, or 20-23 of gestation. Fetal body weights were obtained, and the morphology of the fetal lungs studied by light and electron microscopy. Cytoplasmic volume densities of lamellar inclusion bodies and glycogen within developing type II alveolar epithelial cells were also determined. In addition, total phospholipids (as phosphorus) and glycogen content were determined biochemically. The fetuses from females treated from day 20-23 demonstrated no differences between saline-treated and propranolol-treated groups, in either fetal weight or the morphologic appearance of the developing lung. In contrast, the fetuses from mothers treated from day 18-21 with propranolol were significantly smaller, and their lungs appeared less mature than saline-treated counterparts. The glycogen content of developing type II alveolar epithelial cells was significantly more abundant (as judged by stereologic and biochemical analyses) in the propranolol-treated fetuses. In addition, total phospholipids were decreased in the propranolol-treated 21-day fetuses. The results of the present study suggest that the development of the alveolar epithelium is sensitive to continuous beta-adrenergic blockade by propranolol during a critical time late in gestation.
journal_name
Histol Histopatholjournal_title
Histology and histopathologyauthors
Smith DM,Sommers SSdoi
10.14670/HH-17.365subject
Has Abstractpub_date
2002-04-01 00:00:00pages
365-74issue
2eissn
0213-3911issn
1699-5848journal_volume
17pub_type
杂志文章abstract::During endotoxic shock, the liver exerts a lipopolysaccharide (LPS) clearance function with the participation of both parenchymal and sinusoidal cells. Liver damage could be caused by LPS direct action, hypoxia and/or inflammatory mediators released by Kupffer cells. The aim of this study is to establish an experiment...
journal_title:Histology and histopathology
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doi:
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journal_title:Histology and histopathology
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journal_title:Histology and histopathology
pub_type: 杂志文章
doi:
更新日期:1987-01-01 00:00:00
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journal_title:Histology and histopathology
pub_type: 杂志文章
doi:
更新日期:1997-07-01 00:00:00
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journal_title:Histology and histopathology
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journal_title:Histology and histopathology
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doi:
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journal_title:Histology and histopathology
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journal_title:Histology and histopathology
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journal_title:Histology and histopathology
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journal_title:Histology and histopathology
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