ROLE OF OXYGEN-DERIVED FREE-RADICALS IN FETAL GROWTH-RETARDATION INDUCED BY ISCHEMIA-REPERFUSION IN RATS

We investigated the involvement of oxygen-derived free radicals in the pathogenesis of the intrauterine growth retardation (IUGR) induced in Sprague-Dawley rats by ischemia-reperfusion. On day 17 of gestation, rats received saline, superoxide dismutase (SOD, 50,000 U/kg), catalas e (CAT, 50,000 U/kg), or SOD + CAT subcutaneously 1 h before induction of 30 min of ischemia of the right uterine horn. On day 21 the placen tal level of lipid peroxides was significantly increased (P < 0.001 vs . sham-operated group) and IUGR was induced (P < 0.001 vs. left horn) in the saline-treated group (n = 6). Pretreatment with SOD + CAT (n = 6) significantly inhibited the increase in placental lipid peroxides a nd prevented IUGR. The effect of ischemia-reperfusion on uterine blood flow, with or without pretreatment with radical scavengers, was inves tigated in separate experiments by laser-Doppler flowmetry. The induct ion of hypoperfusion 3 h after ischemia (blood flow -40 +/- 5%, n = 6, P < 0.05) was blocked by pretreatment with SOD + CAT (n = 6). Results indicate that oxygen-derived free radicals may be important in the de velopment of postischemic uteroplacental hypoperfusion and of ischemia -reperfusion-induced IUGR in the rat.