PARENT SESSION
Pregnancy and Parturition

EFFECTS OF ANTENATAL GLUCOCORTICOID (GC) TREATMENT ON THE EYE AND OPTIC NERVE IN THE RAT.

Brown, Jennifer¹, Lempert, Philip¹, Riis, Ronald², Nathanielsz, Peter¹, McDonald, Thomas¹, ^{1 2}

ABSTRACT- INTRODUCTION: Women presenting with preterm delivery are treated with GC to prevent fetal respiratory distress syndrome. The fetal benefits of prenatal GC exposure need to be weighed against possible damage to the developing central nervous system. GC are involved in oligodendrocyte differentiation and regulation of myelin-producing biosynthetic pathways. A recent study in fetal sheep indicates delays in optic nerve axon myelination after repeated betamethasone (M) treatment courses (Maternal-Fetal Medicine, 6:309). The present study investigated antenatal GC effects on rat ocular globe weight (wt), axial eye length and number of myelinated optic nerve axons per field at 30 days (d) of postnatal life. METHODS: Pregnant rats were injected with M (200 or 400 g/kg, sc, once daily) or sterile water on gestational d 15 - 21 (term = 22 d). Pups were allowed to deliver and studied at 30 d postnatal. Ocular globe wts and axial eye lengths were measured and optic nerves fixed. Optic nerve cross sections (3m) were stained (luxol fast blue- cresylecht violet). For all variables, dose levels were compared using ANOVA or t-tests. Results are presented as mean±SEM; n = 4 or 5 rats per treatment group. RESULTS: Ocular globe wts for 400 g/kg animals (0.070±0.004 g) were less than (p < 0.05) those for control and 200 g/kg groups (0.089±0.005 & 0.082±0.003 g, respectively). Axial eye lengths for 200 and 400 g/kg groups (5.6±0.0, and 5.3±0.1 mm, respectively) were less than (p < 0.05) controls (6.3±0.3 mm). The number of myelinated axons per field (625 m²) for the 400 g/kg group (253±14) was reduced (p < 0.05) compared to controls (447±6). CONCLUSIONS: GC administration to fetal rats at doses equal to or greater than those given to pregnant women presenting with preterm labor (approx. 170 g/kg) cause deficits in parameters of the ocular system at 30 d postnatal age i.e., equivalent to the age of puberty (HL 55416).

KEY WORDS: myelination, betamethasone, eye length, ocular development