A study of plasma corticosterone levels in an intrauterine growth restricted rat model at prenatal E19 and postnatal P14

Abstract

A role of fetal exposure to maternal steroids is suggested as a potential mechanism that contributes to the developmental programming of adult CV risk. We hypothesize that the placenta of the IUGR fetus has a higher levels of corticosterone leading to a reduction in placental size and that transmission of maternal steroids to the fetus may serve as a potential mediator of later programmed CV risk. At day 14 gestation RUPP was performed on pregnant rat dams with sham surgeries performed on Control pregnant rat dams. Fetuses were sacrificed at E19 and E20 and P14. Sampling indicated a significant decrease in fetal weight and PW at E19 in the IUGR compared to the Control fetus; PW was significantly decreased at E20 in IUGR compared to Control. However, placental efficiency was significantly higher in IUGR relative to Control at E19 and E20. BW was significantly decreased in IUGR pups compared to Control. A significant increase in plasma levels of corticosterone were observed at E19 in RUPP compared to E19 Control dams; circulating corticosterone levels were also significantly increased in P14 RUPP dams. However, fetal plasma corticosterone levels were not altered in IUGR at E19 compared to Control. In conclusion, early measurements indicated that IUGR fetal weight and weight at birth were significantly reduced by placental insufficiency; however, placental efficiency was increased perhaps indicative of a compensatory mechanism.