EFFECT OF DEXAMETHASONE ON RAT PLASMA PLATELET-ACTIVATING-FACTOR ACETYLHYDROLASE DURING THE PERINATAL-PERIOD

It has been previously reported that the administration of dexamethaso ne (DEX) to adult rats increases the activity of plasma platelet-activ ating factor acetylhydrolase (PAF-AH) and prevents the development of intestinal necrosis caused by platelet activating factor (PAF) injecti on. In this report, we examined the effect of DEX administration on pl asma 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 pla sma PAF-AH activity was lower in late gestation than in postpartum per iod (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 se en in maternal, fetal or neonatal plasma after prenatal DEX administra tion at the aforementioned doses. A higher dose of DEX (1.3 mg/kg/d x 4d) or cortisone (200 mg/kg/d) produced an elevation of maternal plasm a PAF-AH activity (DEX 79.2+/-3.0, cortisone 70.5+/-1.9 vs. controls 4 9.4+/-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 b irth, increased plasma PAF-AH activity on day 4 (DEX 292+/-5 versus co ntrols 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 DE X increases the plasma PAF-AH activity in the rat. Only high doses of prenatal corticosteroids that cause fetal death can elevate maternal p lasma PAF-AH activity.