Published ahead of print on March 18, 2005, doi:10.1164/rccm.200409-1284OC
American Journal of Respiratory and Critical Care Medicine Vol 171. pp. 1395-1402, (2005)
© 2005 American Thoracic Society
doi: 10.1164/rccm.200409-1284OC
Rescue of the Hypoplastic Lung by Prenatal Cyclical Strain
Scott M. Nelson,
Constantinos A. Hajivassiliou,
Graham Haddock,
Alan D. Cameron,
Lindsay Robertson,
Richard E. Olver and
Robert Hume
Division of Maternal and Child Health Sciences, University of Dundee, Dundee; Department of Paediatric Surgery, Royal Hospital for Sick Children and University of Glasgow; Department of Obstetrics and Fetal Medicine, Queen Mother's Hospital; and Department of Veterinary Anatomy, University of Glasgow, Glasgow, Scotland, United Kingdom.
Correspondence and requests for reprints should be addressed to Professor Robert Hume, Maternal and Child Health Sciences, University of Dundee, Ninewells Hospital & Medical School, Dundee, DD1 9SY Scotland UK. E-mail: r.hume{at}dundee.ac.uk
We determined the effects of sustained and cyclical prenatal mechanical strain on the hypoplastic lung of the ovine model of congenital diaphragmatic hernia. Over a period of 4 weeks in late gestation, repeated cyclical tracheal occlusion for 23 hours with 1-hour release stimulated minimal growth, but promoted maturation with the development of a saccular lung. In contrast, a cycle consisting of 47 hours with 1-hour release induced optimal lung growth and morphologic maturation of the hypoplastic lung parenchyma. Sustained occlusion resulted in exaggerated lung growth, exceeding that of unaffected controls, and abnormal alveolar development. The extent of induction of lung growth by mechanical strain was inversely proportional to the number of alveolar type II cells remaining in the lung epithelium. These studies show that, although mechanical strain is capable of inducing lung growth and differentiation, cyclical strain is a prerequisite for normal development and that mechanically induced growth occurs at the expense of the alveolar type II cell. We conclude that cyclical strain may allow optimal alveolar development while maintaining a population of alveolar type II cells and may thus facilitate an improvement in postnatal lung function in infants with congenital diaphragmatic hernia.
Key Words: diaphragmatic hernia • fetoscopy • fetus • lung
This article has been cited by other articles:
|
|
|
|
 
A. Bush
Update in Pediatric Lung Disease 2007
Am. J. Respir. Crit. Care Med.,
April 1, 2008;
177(7):
686 - 695.
[Full Text]
[PDF]
|
|
|
|
|
|
|
Z. Xue, L. Zhang, Y. Liu, S. J. Gunst, and R. S. Tepper
Chronic inflation of ferret lungs with CPAP reduces airway smooth muscle contractility in vivo and in vitro
J Appl Physiol,
March 1, 2008;
104(3):
610 - 615.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
O. Boucherat, A. Benachi, A.-M. Barlier-Mur, M.-L. Franco-Montoya, J. Martinovic, B. Thebaud, B. Chailley-Heu, and J. R. Bourbon
Decreased Lung Fibroblast Growth Factor 18 and Elastin in Human Congenital Diaphragmatic Hernia and Animal Models
Am. J. Respir. Crit. Care Med.,
May 15, 2007;
175(10):
1066 - 1077.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Bush
Update in Pediatric Lung Disease 2006
Am. J. Respir. Crit. Care Med.,
March 15, 2007;
175(6):
532 - 540.
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. C. Featherstone, M. G. Connell, D. G. Fernig, S. Wray, T. V. Burdyga, P. D. Losty, and E. C. Jesudason
Airway Smooth Muscle Dysfunction Precedes Teratogenic Congenital Diaphragmatic Hernia and May Contribute to Hypoplastic Lung Morphogenesis
Am. J. Respir. Cell Mol. Biol.,
November 1, 2006;
35(5):
571 - 578.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. R. Bourbon and A. Benachi
CFTR gene therapy, a method to rescue lung hypoplasia in congenital diaphragmatic hernia?
Am J Physiol Lung Cell Mol Physiol,
July 1, 2006;
291(1):
L1 - L3.
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Bush
Update in pediatrics 2005.
Am. J. Respir. Crit. Care Med.,
March 15, 2006;
173(6):
585 - 592.
[Full Text]
[PDF]
|
|
|
Copyright © 2005 American Thoracic Society
|
|
|
