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Am J Physiol Heart Circ Physiol 272: H701-H705, 1997;
0363-6135/97 $5.00
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AJP - Heart and Circulatory Physiology, Vol 272, Issue 2 701-H705, Copyright © 1997 by American Physiological Society

ARTICLES

Role of oxygen-derived free radicals in free growth retardation induced by ischemia-reperfusion in rats

H. Ishimoto, M. Natori, M. Tanaka, T. Miyazaki, T. Kobayashi and Y. Yoshimura
Department of Obstetrics and Gynecology, Keio University School of Medicine, Tokyo, Japan.

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), catalase (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 placental 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 and prevented IUGR. The effect of ischemia-reperfusion on uterine blood flow, with or without pretreatment with radical scavengers, was investigated in separate experiments by laser-Doppler flowmetry. The induction 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 development of postischemic uteroplacental hypoperfusion and of ischemia-reperfusion-induced IUGR in the rat.


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