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Am J Physiol Heart Circ Physiol 280: H1215-H1221, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 3, H1215-H1221, March 2001

Role of leukocytes in uterine hypoperfusion and fetal growth retardation induced by ischemia-reperfusion

Kei Miyakoshi1, Hitoshi Ishimoto1, Osamu Nishimura1, Shinji Tanigaki1, Mamoru Tanaka1, Toyohiko Miyazaki1, Michiya Natori2, and Yasunori Yoshimura1

1 Department of Obstetrics and Gynecology, Keio University School of Medicine, Tokyo 160-8582; and 2 Department of Clinical Research, National Ohkura Hospital, Tokyo 157-0063, Japan

We investigated leukocyte involvement in uterine hypoperfusion and intrauterine fetal growth retardation (IUGR) induced by ischemia-reperfusion (I/R) in Sprague-Dawley rats. On day 17 of gestation, leukocyte accumulation in the uterus and placenta subjected to 30 min of ischemia, followed by reperfusion, was assessed by measuring myeloperoxidase (MPO) activity. Uterine MPO activity was significantly higher after 1 h of reperfusion than it was before ischemia (P < 0.05), without any increase in placental MPO activity. Immunohistochemical staining showed leukocyte accumulation in the uterus subjected to I/R. The effects of treatment with monoclonal antibodies against CD11a (WT1) and CD18 (WT3) at a dose of 0.8 mg/kg on uterine blood flow and IUGR were investigated. Laser-Doppler flowmetry demonstrated that uterine hypoperfusion at 2 h after ischemia (blood flow, -51.7 ± 1.2%; P < 0.01) was inhibited by WT1 and WT3 treatment. I/R-induced IUGR at full term (P < 0.05 vs. nonischemic horn) was prevented by WT1 and WT3 treatment on day 17. These results indicate that leukocyte accumulation may play an important role in the pathogenesis of uterine hypoperfusion and IUGR induced by I/R in pregnant rats.

uterine blood flow; CD11/CD18 integrin; rat


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