Our purpose was to study the effect of dexamethasone (DEX) on choroidal (ChBF) and retinal blood flow (RBF) during normoxia and hyperoxia. Eighteen spontaneously breathing newborn piglets were examined. ChBF and RBF were measured using radiolabeled microspheres while the piglets were in normoxia before (RA1) and 45 min after either saline or DEX (2 mg/kg) infusion (RA2), and after 90 min of hyperoxia (O2) (Pao2 40-60 kPa). Vitreous prostanoids (prostaglandins F1 alpha and E2 and thromboxane B2) and leukotrienes (leukotriene B4) measurements were obtained during normoxia after either placebo or DEX infusion in an additional 22 piglets. Vitreous prostanoids were also studied after 90 min of hyperoxia. We found that RBF increased significantly after DEX infusion (p < 0.02). There was no change in RBF from RA1 to RA2, before and after saline infusion. RBF decreased significantly during hyperoxia in both groups (p < 0.03). ChBF did not change significantly between RA1 and RA2 in any of the groups. ChBF decreased significantly during hyperoxia in both groups (p < 0.03). Vitreous prostanoids and leukotrienes were reduced significantly after DEX infusion (p < 0.05). Prostanoids were similar in the two groups during hyperoxia. We concluded that DEX increases RBF significantly, but not ChBF. RBF and ChBF decreased in both groups during hyperoxia. Therefore, the metabolites of arachidonic acid do not seem to be involved as mediators of hyperoxic vasoconstriction.