Abstract 319 Poster Session IV, Tuesday, 5/4 (poster 294)

Nitric oxide (NO) is produced after the conversion of L-arginine to L-citrulline by nitric oxide synthase (NOS). The expression pattern of NOS during perinatal period is throught to be involved in transitional circulation after birth. Even though three isoforms of NOS (brain(b), inducible (i), and endothelial (e)) in fetal lungs of late gestation rats have been identified by immunochemistry, only eNOS and bNOS can be detected in the first postnatal week. The expression of eNOS is reduced with the increase of postnatal age. Antenatal dexamethasone elicits beneficial effect of fetal lung development. However, the potential for adverse effects with life-long implication on treated fetuses has been a concern. The purpose of this study was to examine whether antenatal Dex administration altered the expression of eNOS in postnatal lungs of rat pups. The objectives of this study were 1) to characterize the expression of eNOS and iNOS in postnatal lungs, 2) to measure the body weight and lung weight after Dex treatment, and 3) to examine the effect of Dex on the expression of eNOS. Wistar rats of gestational day 18 were subjected with Dex (0.8 mg/kg, im, daily) for two days and then underwent natural delivery. The pups on the day of delivery were assigned as D1. Lungs and brain from D1, 3, 5, 7 pups were used for measuring wet weight and extracting cytosolic protein. As our data indicated, the expression of eNOS from lung and brain was decreased with postnatal age. Postnatal lung expressed much more eNOS than brain. When compared with adult lungs, postnatal pups elicited significantly expression of eNOS at D5 (P < 0.05). No iNOS were detected. Antenatal Dex administration suppressed the expression of eNOS in a time-dependent manner. In conclusion, the expression of eNOS may be involved in transitional circulation. Antenatal Dex may modulate the transitional circulation.