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

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) indu...

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Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 2001-03, Vol.280 (3), p.H1215-H1221
Hauptverfasser: Miyakoshi, Kei, Ishimoto, Hitoshi, Nishimura, Osamu, Tanigaki, Shinji, Tanaka, Mamoru, Miyazaki, Toyohiko, Natori, Michiya, Yoshimura, Yasunori
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container_end_page H1221
container_issue 3
container_start_page H1215
container_title American journal of physiology. Heart and circulatory physiology
container_volume 280
creator Miyakoshi, Kei
Ishimoto, Hitoshi
Nishimura, Osamu
Tanigaki, Shinji
Tanaka, Mamoru
Miyazaki, Toyohiko
Natori, Michiya
Yoshimura, Yasunori
description 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
doi_str_mv 10.1152/ajpheart.2001.280.3.h1215
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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 &lt; 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 &lt; 0.01) was inhibited by WT1 and WT3 treatment. I/R-induced IUGR at full term ( P  &lt; 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</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.2001.280.3.h1215</identifier><identifier>PMID: 11179066</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Antibodies, Monoclonal - pharmacology ; CD18 Antigens - immunology ; Female ; Fetal Growth Retardation - immunology ; Fetal Growth Retardation - pathology ; Fetal Growth Retardation - physiopathology ; Fetal Weight ; Leukocytes - physiology ; Lymphocyte Function-Associated Antigen-1 - immunology ; Organ Size ; Placenta - blood supply ; Placenta - immunology ; Placenta - pathology ; Pregnancy ; Rats ; Reperfusion Injury - immunology ; Reperfusion Injury - pathology ; Reperfusion Injury - physiopathology ; Uterus - blood supply ; Uterus - immunology ; Uterus - physiopathology</subject><ispartof>American journal of physiology. 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Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>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 &lt; 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 &lt; 0.01) was inhibited by WT1 and WT3 treatment. I/R-induced IUGR at full term ( P  &lt; 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</description><subject>Animals</subject><subject>Antibodies, Monoclonal - pharmacology</subject><subject>CD18 Antigens - immunology</subject><subject>Female</subject><subject>Fetal Growth Retardation - immunology</subject><subject>Fetal Growth Retardation - pathology</subject><subject>Fetal Growth Retardation - physiopathology</subject><subject>Fetal Weight</subject><subject>Leukocytes - physiology</subject><subject>Lymphocyte Function-Associated Antigen-1 - immunology</subject><subject>Organ Size</subject><subject>Placenta - blood supply</subject><subject>Placenta - immunology</subject><subject>Placenta - pathology</subject><subject>Pregnancy</subject><subject>Rats</subject><subject>Reperfusion Injury - immunology</subject><subject>Reperfusion Injury - pathology</subject><subject>Reperfusion Injury - physiopathology</subject><subject>Uterus - blood supply</subject><subject>Uterus - immunology</subject><subject>Uterus - physiopathology</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1r3DAQhkVpaTYff6Gol97saKy1ZNFTCU1SCBRKehayNVor9VquZJP638dmNx-XXkYM874zrx5CPgPLAcri0jwMLZo45gVjkBcVy3neQgHlO7JZ5kUGJVfvyYZxwTMBvDwhpyk9MMZKKfhHcgIAUjEhNqT9FTqkwdEOpz-hmUdM1Pd0GjH6Hmk7D2HA6KbkQ09Nb6nD0XR0F8Pj2NK4NNGacR363k4NWlrP1Kemxb03WcQX8zn54EyX8OL4npHf19_vr26zu583P66-3WXNVsKYORC1k5Yv1VkwWBunimprrdpWrhRMFaaEmgs0snBVLYuGg3KcN1yBrNDxM_LlsHeI4e-EadT7JQ52nekxTElLJrZScbUI1UHYxJBSRKeH6PcmzhqYXjHrZ8x6xawXzJrr2xXz4v10PDLVe7SvziPXRfD1IGj9rn30EfXQzguGLuxmfT113T3-G18OvFmtB7v-4fL_7tdUbwI9AQBNpU0</recordid><startdate>20010301</startdate><enddate>20010301</enddate><creator>Miyakoshi, Kei</creator><creator>Ishimoto, Hitoshi</creator><creator>Nishimura, Osamu</creator><creator>Tanigaki, Shinji</creator><creator>Tanaka, Mamoru</creator><creator>Miyazaki, Toyohiko</creator><creator>Natori, Michiya</creator><creator>Yoshimura, Yasunori</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20010301</creationdate><title>Role of leukocytes in uterine hypoperfusion and fetal growth retardation induced by ischemia-reperfusion</title><author>Miyakoshi, Kei ; Ishimoto, Hitoshi ; Nishimura, Osamu ; Tanigaki, Shinji ; Tanaka, Mamoru ; Miyazaki, Toyohiko ; Natori, Michiya ; Yoshimura, Yasunori</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-f16bf7d36bffd1aebaf9284dd948f56092a51b36ea72f8b72c319f33c39178ef3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Antibodies, Monoclonal - pharmacology</topic><topic>CD18 Antigens - immunology</topic><topic>Female</topic><topic>Fetal Growth Retardation - immunology</topic><topic>Fetal Growth Retardation - pathology</topic><topic>Fetal Growth Retardation - physiopathology</topic><topic>Fetal Weight</topic><topic>Leukocytes - physiology</topic><topic>Lymphocyte Function-Associated Antigen-1 - immunology</topic><topic>Organ Size</topic><topic>Placenta - blood supply</topic><topic>Placenta - immunology</topic><topic>Placenta - pathology</topic><topic>Pregnancy</topic><topic>Rats</topic><topic>Reperfusion Injury - immunology</topic><topic>Reperfusion Injury - pathology</topic><topic>Reperfusion Injury - physiopathology</topic><topic>Uterus - blood supply</topic><topic>Uterus - immunology</topic><topic>Uterus - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Miyakoshi, Kei</creatorcontrib><creatorcontrib>Ishimoto, Hitoshi</creatorcontrib><creatorcontrib>Nishimura, Osamu</creatorcontrib><creatorcontrib>Tanigaki, Shinji</creatorcontrib><creatorcontrib>Tanaka, Mamoru</creatorcontrib><creatorcontrib>Miyazaki, Toyohiko</creatorcontrib><creatorcontrib>Natori, Michiya</creatorcontrib><creatorcontrib>Yoshimura, Yasunori</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of physiology. 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Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2001-03-01</date><risdate>2001</risdate><volume>280</volume><issue>3</issue><spage>H1215</spage><epage>H1221</epage><pages>H1215-H1221</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><abstract>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 &lt; 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 &lt; 0.01) was inhibited by WT1 and WT3 treatment. I/R-induced IUGR at full term ( P  &lt; 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</abstract><cop>United States</cop><pmid>11179066</pmid><doi>10.1152/ajpheart.2001.280.3.h1215</doi></addata></record>
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subjects Animals
Antibodies, Monoclonal - pharmacology
CD18 Antigens - immunology
Female
Fetal Growth Retardation - immunology
Fetal Growth Retardation - pathology
Fetal Growth Retardation - physiopathology
Fetal Weight
Leukocytes - physiology
Lymphocyte Function-Associated Antigen-1 - immunology
Organ Size
Placenta - blood supply
Placenta - immunology
Placenta - pathology
Pregnancy
Rats
Reperfusion Injury - immunology
Reperfusion Injury - pathology
Reperfusion Injury - physiopathology
Uterus - blood supply
Uterus - immunology
Uterus - physiopathology
title Role of leukocytes in uterine hypoperfusion and fetal growth retardation induced by ischemia-reperfusion
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