The skin surface of the newborn rat at term is highly hydrophobic. Thi
s surface hydrophobicity plays a putative role in the transition from
an aqueous to a gaseous environment at birth and is dependent on the p
resence of an intact periderm. Glucocorticoids given to pregnant dams,
during late gestation, will accelerate formation of the stratum corne
um and reduce transepidermal water loss in prematurely delivered pups.
We tested the related hypotheses that surface hydrophobicity and matu
ration of the periderm are developmentally accelerated by prenatal exp
osure to steroids. Thirty pregnant Sprague-Dawley rats received either
normal saline or 0.5 mg/kg betamethasone on d 17 of gestation. After
cesarean delivery on d 18, 19, and 20, dorsal skin surface hydrophobic
ity was quantified by direct surface electrical capacitance (SEC) meas
urement. Initial skin surface hydration at birth was significantly low
er in steroid-treated pups than in control pups at gestational ages 19
and 20 d (3060 +/- 1379 versus 4441 +/- 153 pF and 646 +/- 295 versus
1493 +/- 1019 pF, respectively, p < 0.001, mean +/- SD). Likewise, af
ter desorption of amniotic fluid, baseline skin hydration was signific
antly lower in steroid-treated pups than in control pups at gestationa
l ages 19 and 20 d (1862 +/- 1560 pF versus 4278 +/- 97 pF and 60 +/-
56 pF versus 128 +/- 264 pF, p < 0.001). Scanning and transmission ele
ctron microscopy showed morphologic maturation of the periderm after s
teroid treatment. These results demonstrate accelerated development of
both functional and structural correlates of skin surface hydrophobic
ity in the premature rat after prenatal exposure to steroids.