Abstract

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.

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