Fetal lung growth depends on the degree to which lungs are distended w
ith luminal liquid. Fetal lungs are highly distended such that mean lu
minal volume exceeds the static relaxation volume. This high level of
expansion is maintained by fetal breathing movements and by resistive
effects of the upper airway during apnea; both factors oppose lung rec
oil. Mechanical stress in lung and other tissues stimulates cell divis
ion and tissue remodeling. Potential transduction mechanisms involve d
irect effects of cellular tension and mediation of locally released mi
togenic factors. Further studies are required to further define links
between lung tissue stress, increased growth, structural remodeling, a
nd the endocrine environment. A common cause of fetal lung hypoplasia
is a sustained reduction in mean lung expansion. Studies of mechanisms
controlling fetal lung expansion have led to insights into the etiolo
gy of fetal lung hypoplasia and how it may be remedied in utero. Fetal
lung hypoplasia can have long-lasting effects on postnatal lung funct
ion, as airway and alveolar formation may be compromised. Preterm birt
h may also result in incomplete structural development of the lungs as
it shortens the period of increased intrauterine lung expansion.