Document Detail


The effects of mechanical forces on fetal lung growth.
MedLine Citation:
PMID:  8982567     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Abnormalities of fetal lung growth, especially pulmonary hypoplasia, are important causes of neonatal morbidity and mortality. For most clinical conditions associated with abnormal lung growth, studies in experimental animals indicate that these conditions affect the mechanical forces acting on the fetal lung. The major stimulus to growth in the fetal lung is stretch, which is due either to (1) to the constant distending pressure during periods when fetal breathing movements are absent, or (2) the intermittent, repetitive stretch induced by changes in thoracic shape during fetal breathing movements. The mechanisms by which stretch is transduced to a biochemical signal stimulating cell division have not been defined. There are some indications that the mechanical forces that influence lung growth may also affect surfactant, but further studies are needed to define these effects and their possible clinical significance.
Authors:
J A Kitterman
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Clinics in perinatology     Volume:  23     ISSN:  0095-5108     ISO Abbreviation:  Clin Perinatol     Publication Date:  1996 Dec 
Date Detail:
Created Date:  1997-03-26     Completed Date:  1997-03-26     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  7501306     Medline TA:  Clin Perinatol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  727-40     Citation Subset:  IM    
Affiliation:
Cardiovascular Research Institute, University of California, San Francisco, USA. Jkitterm@PEDS.ucsf.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Biomechanics
Fetal Organ Maturity / physiology
Fetus / physiology
Lung / embryology*
Grant Support
ID/Acronym/Agency:
HL-24075/HL/NHLBI NIH HHS

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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