Glucocorticoids (GC) reduce chronic lung disease (CLD) in premature infants. However, studies have raised concern because of adverse effects of GC on somatic growth and organ development¹. Treatment of neonatal rats with dexamethasone (Dex) promotes adverse effects on heart structure and function in adulthood². In humans, GC excess increases superoxide production and vascular dysfunction, effects that are resolved by vitamin C³. The aims of this study were to determine in rats: 1) the effects of neonatal Dex administration on early somatic growth and heart development, and 2) whether co-administration with vitamins C and E ameliorates any detrimental effects of GC. Male Wistar pups received i.p. injections of Dexamethasone-21-phosphate (Dex; n = 7; 0.5, 0.3, 0.1 µg.g^-1) or Dex with vitamins C and E (DCE; n = 12; 200 mg.kg^-1 and 100 mg.kg^-1, respectively) on postnatal days 1-3 (P1-3); vitamins were continued from P4-6. Controls received equal volumes (10 ml.kg^-1) of saline (ctrl; n = 11) from P1-6. The tapering course of Dex used was adopted from a human clinical regimen used in preterm infants⁴. The doses of vitamins were adopted from studies in rats which showed successful antioxidant effects⁵. On P21, following euthanasia (0.2 mL, i.p., xylazine and ketamine), biometry measurements were taken and hearts were snap frozen for protein analysis. Antibodies against eNOS, Hsp90, and 4-hydroxynonenal (4-HNE) were used to assess oxidant stress. Data were analyzed by One-Way ANOVA + Tukey and chi-square test. Compared to controls, Dex treatment reduced survival (ctrl: 96%; Dex: 70%, P<0.05), and promoted postnatal asymmetric growth restriction (body weight (BW) at P21 ctrl: 65.1 ± 2.7 vs. Dex: 50.9 ± 1.1 g, Ponderal index (PI) at P21 ctrl: 6.3 ± 0.1 vs. Dex: 7.4 ± 0.2 kg.m^-3, P<0.05). Western blot analysis revealed that, compared to controls, Dex increased 4-HNE (13%) whilst decreasing Hsp90 (-42%) and eNOS (-54%) expression (P<0.05). Addition of vitamins to Dex pups increased survival (DCE: 93%) and restored PI to control levels (6.7 ± 0.1 kg.m^-3, P<0.05), but did not alter the reduction in BW. In DCE pups, eNOS protein was restored to control levels and Hsp90 was reduced to a lesser extent (-22%), while 4-HNE remained upregulated (22%). In conclusion, Dex treatment of neonatal rats has detrimental effects on somatic growth and survival and promotes a decrease in proteins that may lead to increased oxidant stress and decreased NO bioavailability in the neonatal heart. Addition of antioxidant vitamins to Dex-treated pups ameliorates these effects. This study raises the possibility that combined treatment of premature infants with GC and antioxidants may be better than administration of GC alone in the treatment of CLD.