Oligohydramnios is known to cause pulmonary hypoplasia. Previous experiments have shown that the maturation of lungs of fetal rats subjected to oligohydramnios is similar to control animals as measured by DNA, protein and phospholipid concentrations, and surface area to lung weight ratio. We have previously reported that apoptosis occurs in the fetal rat lung in late gestation; because apoptotic cells were seen only in the interstitium, we postulated that apoptosis aids in the maturational process of interstitial thinning. The aim of the present study was to determine if oligohydramnios affects apoptosis in the developing fetal rat lung.

Oligohydramnios was produced in fetal rats by puncturing the uterine wall and fetal membranes of one uterine horn at 16 d gestation using a 22 Ga needle. Contralateral fetuses were matched by position and served as controls. Under general anesthesia, fetuses were delivered by hysterotomy at 20, 21 and 22 d gestation, and their lungs were removed and fixed in paraformaldehyde. We studied 2 fetal pairs at each gestational age. Fetal and lung weights were obtained in 1 pair at each gestation and confirmed that oligohydramnios produced pulmonary hypoplasia. Using in situ end labeling of DNA with biotinylated ATP tagged with fluorescein to identify apoptotic cells, we calculated the apoptotic index (AI, AI = number of apoptotic cells / 1000 nuclei) for each gestation. The AI ranged from 1.98 to 6.69, and showed no difference between fetuses with oligohydramnios and their controls.

We conclude that oligohydramnios does not affect the rate of apoptosis in the lungs of fetal rats in late gestation. These findings are consistent with prior studies indicating that oligohydramnios causes decreased lung growth, but does not affect lung maturation.

Supported by National Heart, Lung and Blood Institute Grant HL-24075.