Role of oxygen-derived free radicals in fetal growth retardation
induced by ischemia-reperfusion in rats.
Ishimoto, Hitoshi, Michiya Natori, Mamoru Tanaka, Toyohiko Miyazaki,
Toshifumi Kobayashi, and Yasunori Yoshimura.
Department of Obstetrics and Gynecology, Keio University School of
Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160; and Department of
Clinical Research, National Ohkura Hospital, 2-10-1 Ohkura, Setagaya
-ku, Tokyo 157, Japan
APStracts 3:0371H, 1996.
We investigated the involvement of oxygen-derived free radicals (OFR)
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; 50000
U/kg), catalase (CAT; 50000 U/kg), or SOD+CAT sc one h before
induction of 30-min 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 (BF), with or without
pretreatment with radical scavengers, was investigated in separate
experiments by laser-Doppler flowmetry. The induction of
hypoperfusion 3 h after ischemia (BF -40 [umlaut]u} 5%, n = 6, P
< 0.05) was blocked by pretreatment with SOD+CAT (n = 6).
Results indicate that OFR may be important in the development of
postischemic uteroplacental hypoperfusion and of ischemia
-reperfusion-induced IUGR in the rat.
Received 22 February 1996; accepted in final form 26 August 1996.
APS Manuscript Number H177-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996