Effect of dexamethasone on rat plasma platelet activating factor acetylhydrolase during the perinatal period

Document Type

Journal Article

Publication Date



Early Human Development








Dexamethasone; Necrotizing enterocolitis; PAF-acetylhydrolase; Platelet activating factor


It has been previously reported that the administration of dexamethasone (DEX) to adult rats increases the activity of plasma platelet-activating factor acetylhydrolase (PAF-AH) and prevents the development of intestinal necrosis caused by platelet activating factor (PAF) injection. In this report, we examined the effect of DEX administration on plasma PAF-AH activity during the perinatal period. Timed-pregnant rats received DEX (0.2-1.0 mg/kg/d) or normal saline (controls) on days 16-18 (early group) or days 18-20 (late group) of gestation. Maternal plasma PAF-AH activity was lower in late gestation than in postpartum period (P < 0.001). Fetal and neonatal plasma PAF-AH activity was higher than maternal values (P < 0.05). No changes of PAF-AH activity were seen in maternal, fetal or neonatal plasma after prenatal DEX administration at the aforementioned doses. A higher dose of DEX (1.3 mg/kg/d x 4 d) or cortisone (200 mg/kg/d) produced an elevation of maternal plasma PAF-AH activity (DEX 79.2 ± 3.0, cortisone 70.5 ± 1.9 vs. controls 49.4 ± 2.3 nmol/min/ml, P < 0.01), but resulted in a high fetal mortality. Treatment of newborn rats with DEX (0.5 mg/kg/d) on days 1-3 after birth, increased plasma PAF-AH activity on day 4 (DEX 292 ± 5 versus controls 140 ± 9 nmol/min/ml, P < 0.001) and day 6 (DEX 302 ± 12 versus controls 136 ± 6 nmol/min/ml, P < 0.001). Postnatal administration of DEX increases the plasma PAF-AH activity in the rat. Only high doses of prenatal corticosteroids that cause fetal death can elevate maternal plasma PAF-AH activity.

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