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3 Medical Research Council Group in Fetal and Neonatal Health and Development and Departments of 1 Obstetrics and Gynaecology, 2 Physiology, and 4 Biochemistry, The Lawson Research Institute, St. Joseph's Health Centre, and London Health Sciences Centre, The University of Western Ontario, London, Ontario, Canada N6A 4V2
To test the hypothesis that chronic placental
insufficiency resulting in fetal growth restriction causes an increase
in fetal lung surfactant-associated protein (SP) gene expression, we
embolized chronically catheterized fetal sheep
(n = 6) daily using nonradioactive microspheres in the abdominal aorta for 21 days (between 0.74 and 0.88 of gestation) until fetal arterial oxygen content was reduced by
~40-50%. Control animals (n = 7) received saline only. Basal fetal plasma cortisol
concentration was monitored. At the end of the experiment, fetal lung
tissues were collected, and ratios of tissue levels of SP-A, SP-B, and
SP-C mRNA to 18S rRNA were determined by standard Northern blot
analysis. Total DNA content of fetal lungs was reduced by 30% in the
embolized group compared with control group
(P = 0.01). There was a 2.7-fold
increase in fetal lung SP-A mRNA (P < 0.05) and a 3.2-fold increase in SP-B mRNA
(P < 0.01) in the chronically
embolized group compared with those in the control group. SP-A and SP-B
mRNA tissue levels were highly correlated with the mean fetal plasma
cortisol levels on days 20-21
(r = 0.90, P < 0.01 for SP-A mRNA and
r = 0.94, P < 0.01 for SP-B mRNA). SP-C mRNA
tissue levels were not significantly affected by placental
insufficiency. We conclude that fetal growth restriction due to
placental insufficiency is associated with alterations in fetal lung
SP, suggesting enhanced lung maturation that was highly dependent on
the degree of increase in fetal plasma cortisol levels.
fetal growth retardation; placental insufficiency; glucocorticoids; surfactant apoprotein expression
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