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PARENT SESSION
Pregnancy and Parturition


596

PRENATAL BETAMETHASONE (M) FROM 68 - 77 % OF GESTATION REDUCES RAT FETAL AND PLACENTAL WEIGHTS .

Franko, Kate1, Nathanielsz, Peter1, McDonald, Thomas1, 1

ABSTRACT- Introduction: Fetal benefits of antenatal glucocorticoids (GC) given to women with preterm labor are well known (e.g., prevention of respiratory distress syndrome), however concern exists regarding potentially harmful side effects. We previously demonstrated that in rats given M (100 g/kg/day; s.c.) over the last 7 days of pregnancy, placental weight (wt) is decreased and pup:placental wt is increased at 21 days of gestation without a change in pup wt (Soc.Gyn. Invest. 47th Ann. Mtg.). The present study investigated GC administration from days 68 - 77 % (15-17 days) of pregnancy on fetal and placental wts. Methods: Pregnant Sprague-Dawley rats were given s.c. injections of saline (control, n = 8) or 100 g/kg of M (n = 7) once per day on days 15-17 of pregnancy at 10:00 am. At 14:00 on day 17, all rats were killed by CO2 inhalation and pup and placental wts were recorded. Results: There were no differences between groups in number of pups per litter. Average pup and placental wts were larger (p < 0.05) in controls (1.16±0.09 and 0.49±0.03 g, mean±SEM, respectively) than in M (0.9±0.03 and 0.38±0.02 g, respectively) exposed animals while pup:placenta wts were not different. Conclusions: In rats, M treatment from 68 to 77 % of pregnancy at doses lower than those given to pregnant women presenting with preterm labor (NIH Consensus Statement, 1994) causes growth retardation equally of both the fetus and the placenta. The results of the present study coupled with those of our previous report mentioned above indicate that the fetus, but not the placenta, exhibits compensatory growth when exposed to GC in the last third of pregnancy. However there may be a cost for this compensatory growth since epidemiological data (Mothers, Babies and Health in Later Life, Churchill Livingstone, NY, 1998) suggest that imbalances in the fetal-placental ratio are prognosticators of adult cardiovascular disease. We conclude that further examination of the mechanisms and adult consequences of GC influences on fetal and placental growth are needed to evaluate the importance of these findings. (Supported by HL65399)

KEY WORDS: antenatal glucocorticoids, placenta, growth


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